Module 6: The Lymphatic and Immune Systems

Lesson 3: The Adaptive Immune Response: T-lymphocytes and Their Functional Types

Đáp Ứng Miễn Dịch Thích Nghi: Tế Bào Lympho T Và Các Dạng Chức Năng

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Dưới đây là danh sách những thuật ngữ Y khoa của module The Lymphatic and Immune Systems.
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Medical Terminology: The Lymphatic and Immune Systems

active immunity
immunity developed from an individual’s own immune system
acute inflammation
inflammation occurring for a limited time period; rapidly developing
adaptive immune response
relatively slow but very specific and effective immune response controlled by lymphocytes
afferent lymphatic vessels
lead into a lymph node
antibody
antigen-specific protein secreted by plasma cells; immunoglobulin
antigen
molecule recognized by the receptors of B and T lymphocytes
antigen presentation
binding of processed antigen to the protein-binding cleft of a major histocompatibility complex molecule
antigen processing
internalization and digestion of antigen in an antigen-presenting cell
antigen receptor
two-chain receptor by which lymphocytes recognize antigen
antigenic determinant
(also, epitope) one of the chemical groups recognized by a single type of lymphocyte antigen receptor
B cells
lymphocytes that act by differentiating into an antibody-secreting plasma cell
barrier defenses
antipathogen defenses deriving from a barrier that physically prevents pathogens from entering the body to establish an infection
bone marrow
tissue found inside bones; the site of all blood cell differentiation and maturation of B lymphocytes
bronchus-associated lymphoid tissue (BALT)
lymphoid nodule associated with the respiratory tract
central tolerance
B cell tolerance induced in immature B cells of the bone marrow
chemokine
soluble, long-range, cell-to-cell communication molecule
chronic inflammation
inflammation occurring for long periods of time
chyle
lipid-rich lymph inside the lymphatic capillaries of the small intestine
cisterna chyli
bag-like vessel that forms the beginning of the thoracic duct
class switching
ability of B cells to change the class of antibody they produce without altering the specificity for antigen
clonal anergy
process whereby B cells that react to soluble antigens in bone marrow are made nonfunctional
clonal deletion
removal of self-reactive B cells by inducing apoptosis
clonal expansion
growth of a clone of selected lymphocytes
clonal selection
stimulating growth of lymphocytes that have specific receptors
clone
group of lymphocytes sharing the same antigen receptor
complement
enzymatic cascade of constitutive blood proteins that have antipathogen effects, including the direct killing of bacteria
constant region domain
part of a lymphocyte antigen receptor that does not vary much between different receptor types
cytokine
soluble, short-range, cell-to-cell communication molecule
cytotoxic T cells (Tc)
T lymphocytes with the ability to induce apoptosis in target cells
delayed hypersensitivity
(type IV) T cell-mediated immune response against pathogens infiltrating interstitial tissues, causing cellular infiltrate
early induced immune response
includes antimicrobial proteins stimulated during the first several days of an infection
effector T cells
immune cells with a direct, adverse effect on a pathogen
efferent lymphatic vessels
lead out of a lymph node
erythroblastosis fetalis
disease of Rh factor-positive newborns in Rh-negative mothers with multiple Rh-positive children; resulting from the action of maternal antibodies against fetal blood
fas ligand
molecule expressed on cytotoxic T cells and NK cells that binds to the fas molecule on a target cell and induces it do undergo apoptosis
Fc region
in an antibody molecule, the site where the two termini of the heavy chains come together; many cells have receptors for this portion of the antibody, adding functionality to these molecules
germinal centers
clusters of rapidly proliferating B cells found in secondary lymphoid tissues
graft-versus-host disease
in bone marrow transplants; occurs when the transplanted cells mount an immune response against the recipient
granzyme
apoptosis-inducing substance contained in granules of NK cells and cytotoxic T cells
heavy chain
larger protein chain of an antibody
helper T cells (Th)
T cells that secrete cytokines to enhance other immune responses, involved in activation of both B and T cell lymphocytes
high endothelial venules
vessels containing unique endothelial cells specialized to allow migration of lymphocytes from the blood to the lymph node
histamine
vasoactive mediator in granules of mast cells and is the primary cause of allergies and anaphylactic shock
IgA
antibody whose dimer is secreted by exocrine glands, is especially effective against digestive and respiratory pathogens, and can pass immunity to an infant through breastfeeding
IgD
class of antibody whose only known function is as a receptor on naive B cells; important in B cell activation
IgE
antibody that binds to mast cells and causes antigen-specific degranulation during an allergic response
IgG
main blood antibody of late primary and early secondary responses; passed from carrier to unborn child via placenta
IgM
antibody whose monomer is a surface receptor of naive B cells; the pentamer is the first antibody made blood plasma during primary responses
immediate hypersensitivity
(type I) IgE-mediated mast cell degranulation caused by crosslinking of surface IgE by antigen
immune system
series of barriers, cells, and soluble mediators that combine to response to infections of the body with pathogenic organisms
immunoglobulin
protein antibody; occurs as one of five main classes
immunological memory
ability of the adaptive immune response to mount a stronger and faster immune response upon re-exposure to a pathogen
inflammation
basic innate immune response characterized by heat, redness, pain, and swelling
innate immune response
rapid but relatively nonspecific immune response
interferons
early induced proteins made in virally infected cells that cause nearby cells to make antiviral proteins
light chain
small protein chain of an antibody
lymph
fluid contained within the lymphatic system
lymph node
one of the bean-shaped organs found associated with the lymphatic vessels
lymphatic capillaries
smallest of the lymphatic vessels and the origin of lymph flow
lymphatic system
network of lymphatic vessels, lymph nodes, and ducts that carries lymph from the tissues and back to the bloodstream.
lymphatic trunks
large lymphatics that collect lymph from smaller lymphatic vessels and empties into the blood via lymphatic ducts
lymphocytes
white blood cells characterized by a large nucleus and small rim of cytoplasm
lymphoid nodules
unencapsulated patches of lymphoid tissue found throughout the body
macrophage
ameboid phagocyte found in several tissues throughout the body
macrophage oxidative metabolism
metabolism turned on in macrophages by T cell signals that help destroy intracellular bacteria
major histocompatibility complex (MHC)
gene cluster whose proteins present antigens to T cells
mast cell
cell found in the skin and the lining of body cells that contains cytoplasmic granules with vasoactive mediators such as histamine
memory T cells
long-lived immune cell reserved for future exposure to a pathogen
MHC class I
found on most cells of the body, it binds to the CD8 molecule on T cells
MHC class II
found on macrophages, dendritic cells, and B cells, it binds to CD4 molecules on T cells
MHC polygeny
multiple MHC genes and their proteins found in body cells
MHC polymorphism
multiple alleles for each individual MHC locus
monocyte
precursor to macrophages and dendritic cells seen in the blood
mucosa-associated lymphoid tissue (MALT)
lymphoid nodule associated with the mucosa
naïve lymphocyte
mature B or T cell that has not yet encountered antigen for the first time
natural killer cell (NK)
cytotoxic lymphocyte of innate immune response
negative selection
selection against thymocytes in the thymus that react with self-antigen
neutralization
inactivation of a virus by the binding of specific antibody
neutrophil
phagocytic white blood cell recruited from the bloodstream to the site of infection via the bloodstream
opsonization
enhancement of phagocytosis by the binding of antibody or antimicrobial protein
passive immunity
transfer of immunity to a pathogen to an individual that lacks immunity to this pathogen usually by the injection of antibodies
pattern recognition receptor (PRR)
leukocyte receptor that binds to specific cell wall components of different bacterial species
perforin
molecule in NK cell and cytotoxic T cell granules that form pores in the membrane of a target cell
peripheral tolerance
mature B cell made tolerant by lack of T cell help
phagocytosis
movement of material from the outside to the inside of the cells via vesicles made from invaginations of the plasma membrane
plasma cell
differentiated B cell that is actively secreting antibody
polyclonal response
response by multiple clones to a complex antigen with many determinants
positive selection
selection of thymocytes within the thymus that interact with self, but not non-self, MHC molecules
primary adaptive response
immune system’s response to the first exposure to a pathogen
primary lymphoid organ
site where lymphocytes mature and proliferate; red bone marrow and thymus gland
psychoneuroimmunology
study of the connections between the immune, nervous, and endocrine systems
regulatory T cells (Treg)
(also, suppressor T cells) class of CD4 T cells that regulates other T cell responses
right lymphatic duct
drains lymph fluid from the upper right side of body into the right subclavian vein
secondary adaptive response
immune response observed upon re-exposure to a pathogen, which is stronger and faster than a primary response
secondary lymphoid organs
sites where lymphocytes mount adaptive immune responses; examples include lymph nodes and spleen
sensitization
first exposure to an antigen
seroconversion
clearance of pathogen in the serum and the simultaneous rise of serum antibody
severe combined immunodeficiency disease (SCID)
genetic mutation that affects both T cell and B cell arms of the immune response
spleen
secondary lymphoid organ that filters pathogens from the blood (white pulp) and removes degenerating or damaged blood cells (red pulp)
T cell
lymphocyte that acts by secreting molecules that regulate the immune system or by causing the destruction of foreign cells, viruses, and cancer cells
T cell tolerance
process during T cell differentiation where most T cells that recognize antigens from one’s own body are destroyed
T cell-dependent antigen
antigen that binds to B cells, which requires signals from T cells to make antibody
T cell-independent antigen
binds to B cells, which do not require signals from T cells to make antibody
Th1 cells
cells that secrete cytokines that enhance the activity of macrophages and other cells
Th2 cells
cells that secrete cytokines that induce B cells to differentiate into antibody-secreting plasma cells
thoracic duct
large duct that drains lymph from the lower limbs, left thorax, left upper limb, and the left side of the head
thymocyte
immature T cell found in the thymus
thymus
primary lymphoid organ; where T lymphocytes proliferate and mature
tissue typing
typing of MHC molecules between a recipient and donor for use in a potential transplantation procedure
tonsils
lymphoid nodules associated with the nasopharynx
type I hypersensitivity
immediate response mediated by mast cell degranulation caused by the crosslinking of the antigen-specific IgE molecules on the mast cell surface
type II hypersensitivity
cell damage caused by the binding of antibody and the activation of complement, usually against red blood cells
type III hypersensitivity
damage to tissues caused by the deposition of antibody-antigen (immune) complexes followed by the activation of complement
variable region domain
part of a lymphocyte antigen receptor that varies considerably between different receptor types
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Innate immune responses (and early induced responses) are in many cases ineffective at completely controlling pathogen growth. However, they slow pathogen growth and allow time for the adaptive immune response to strengthen and either control or eliminate the pathogen. The innate immune system also sends signals to the cells of the adaptive immune system, guiding them in how to attack the pathogen. Thus, these are the two important arms of the immune response.
The specificity of the adaptive immune response—its ability to specifically recognize and make a response against a wide variety of pathogens—is its great strength. Antigens, the small chemical groups often associated with pathogens, are recognized by receptors on the surface of B and T lymphocytes. The adaptive immune response to these antigens is so versatile that it can respond to nearly any pathogen. This increase in specificity comes because the adaptive immune response has a unique way to develop as many as 1012, or 100 trillion, different receptors to recognize nearly every conceivable pathogen. How could so many different types of antibodies be encoded? And what about the many specificities of T cells? There is not nearly enough DNA in a cell to have a separate gene for each specificity. The mechanism was finally worked out in the 1970s and 1980s using the new tools of molecular genetics.

A. Primary Disease and Immunological Memory

The immune system’s first exposure to a pathogen is called a primary adaptive response. Symptoms of a first infection, called primary disease, are always relatively severe because it takes time for an initial adaptive immune response to a pathogen to become effective.

Upon re-exposure to the same pathogen, a secondary adaptive immune response is generated, which is stronger and faster than the primary response. The secondary adaptive response often eliminates a pathogen before it can cause significant tissue damage or any symptoms. Without symptoms, there is no disease, and the individual is not even aware of the infection. This secondary response is the basis of immunological memory, which protects us from getting diseases repeatedly from the same pathogen. By this mechanism, an individual’s exposure to pathogens early in life spares the person from these diseases later in life.

B. Self Recognition

A third important feature of the adaptive immune response is its ability to distinguish between self-antigens, those that are normally present in the body, and foreign antigens, those that might be on a potential pathogen. As T and B cells mature, there are mechanisms in place that prevent them from recognizing self-antigen, preventing a damaging immune response against the body. These mechanisms are not 100 percent effective, however, and their breakdown leads to autoimmune diseases, which will be discussed later in this article.
The primary cells that control the adaptive immune response are the lymphocytes, the T and B cells. T cells are particularly important, as they not only control a multitude of immune responses directly, but also control B cell immune responses in many cases as well. Thus, many of the decisions about how to attack a pathogen are made at the T cell level, and knowledge of their functional types is crucial to understanding the functioning and regulation of adaptive immune responses as a whole.

T lymphocytes recognize antigens based on a two-chain protein receptor. The most common and important of these are the alpha-beta T cell receptors (Figure 1).

There are two chains in the T cell receptor, and each chain consists of two domains. The variable region domain is furthest away from the T cell membrane and is so named because its amino acid sequence varies between receptors. In contrast, the constant region domain has less variation. The differences in the amino acid sequences of the variable domains are the molecular basis of the diversity of antigens the receptor can recognize. Thus, the antigen-binding site of the receptor consists of the terminal ends of both receptor chains, and the amino acid sequences of those two areas combine to determine its antigenic specificity. Each T cell produces only one type of receptor and thus is specific for a single particular antigen.
Antigens on pathogens are usually large and complex, and consist of many antigenic determinants. An antigenic determinant (epitope) is one of the small regions within an antigen to which a receptor can bind, and antigenic determinants are limited by the size of the receptor itself. They usually consist of six or fewer amino acid residues in a protein, or one or two sugar moieties in a carbohydrate antigen. Antigenic determinants on a carbohydrate antigen are usually less diverse than on a protein antigen. Carbohydrate antigens are found on bacterial cell walls and on red blood cells (the ABO blood group antigens). Protein antigens are complex because of the variety of three-dimensional shapes that proteins can assume, and are especially important for the immune responses to viruses and worm parasites. It is the interaction of the shape of the antigen and the complementary shape of the amino acids of the antigen-binding site that accounts for the chemical basis of specificity (Figure 2).

A. Antigen Processing and Presentation

Although Figure 2 shows T cell receptors interacting with antigenic determinants directly, the mechanism that T cells use to recognize antigens is, in reality, much more complex. T cells do not recognize free-floating or cell-bound antigens as they appear on the surface of the pathogen. They only recognize antigen on the surface of specialized cells called antigen-presenting cells. Antigens are internalized by these cells. Antigen processing is a mechanism that enzymatically cleaves the antigen into smaller pieces. The antigen fragments are then brought to the cell’s surface and associated with a specialized type of antigen-presenting protein known as a major histocompatibility complex (MHC) molecule. The MHC is the cluster of genes that encode these antigen-presenting molecules. The association of the antigen fragments with an MHC molecule on the surface of a cell is known as antigen presentation and results in the recognition of antigen by a T cell. This association of antigen and MHC occurs inside the cell, and it is the complex of the two that is brought to the surface. The peptide-binding cleft is a small indentation at the end of the MHC molecule that is furthest away from the cell membrane; it is here that the processed fragment of antigen sits. MHC molecules are capable of presenting a variety of antigens, depending on the amino acid sequence, in their peptide-binding clefts. It is the combination of the MHC molecule and the fragment of the original peptide or carbohydrate that is actually physically recognized by the T cell receptor (Figure 3).

Two distinct types of MHC molecules, MHC class I and MHC class II, play roles in antigen presentation. Although produced from different genes, they both have similar functions. They bring processed antigen to the surface of the cell via a transport vesicle and present the antigen to the T cell and its receptor. Antigens from different classes of pathogens, however, use different MHC classes and take different routes through the cell to get to the surface for presentation. The basic mechanism, though, is the same. Antigens are processed by digestion, are brought into the endomembrane system of the cell, and then are expressed on the surface of the antigen-presenting cell for antigen recognition by a T cell. Intracellular antigens are typical of viruses, which replicate inside the cell, and certain other intracellular parasites and bacteria. These antigens are processed in the cytosol by an enzyme complex known as the proteasome and are then brought into the endoplasmic reticulum by the transporter associated with antigen processing (TAP) system, where they interact with class I MHC molecules and are eventually transported to the cell surface by a transport vesicle.

Extracellular antigens, characteristic of many bacteria, parasites, and fungi that do not replicate inside the cell’s cytoplasm, are brought into the endomembrane system of the cell by receptor-mediated endocytosis. The resulting vesicle fuses with vesicles from the Golgi complex, which contain pre-formed MHC class II molecules. After fusion of these two vesicles and the association of antigen and MHC, the new vesicle makes its way to the cell surface.

B. Professional Antigen-presenting Cells

Many cell types express class I molecules for the presentation of intracellular antigens. These MHC molecules may then stimulate a cytotoxic T cell immune response, eventually destroying the cell and the pathogen within. This is especially important when it comes to the most common class of intracellular pathogens, the virus. Viruses infect nearly every tissue of the body, so all these tissues must necessarily be able to express class I MHC or no T cell response can be made.

On the other hand, class II MHC molecules are expressed only on the cells of the immune system, specifically cells that affect other arms of the immune response. Thus, these cells are called “professional” antigen-presenting cells to distinguish them from those that bear class I MHC. The three types of professional antigen presenters are macrophages, dendritic cells, and B cells (Table 1).

Macrophages stimulate T cells to release cytokines that enhance phagocytosis. Dendritic cells also kill pathogens by phagocytosis (see Figure 3), but their major function is to bring antigens to regional draining lymph nodes. The lymph nodes are the locations in which most T cell responses against pathogens of the interstitial tissues are mounted. Macrophages are found in the skin and in the lining of mucosal surfaces, such as the nasopharynx, stomach, lungs, and intestines. B cells may also present antigens to T cells, which are necessary for certain types of antibody responses, to be covered later in this chapter.
The process of eliminating T cells that might attack the cells of one’s own body is referred to as T cell tolerance. While thymocytes are in the cortex of the thymus, they are referred to as “double negatives,” meaning that they do not bear the CD4 or CD8 molecules that you can use to follow their pathways of differentiation (Figure 4). In the cortex of the thymus, they are exposed to cortical epithelial cells. In a process known as positive selection, double-negative thymocytes bind to the MHC molecules they observe on the thymic epithelia, and the MHC molecules of “self” are selected. This mechanism kills many thymocytes during T cell differentiation. In fact, only two percent of the thymocytes that enter the thymus leave it as mature, functional T cells.

Later, the cells become double positives that express both CD4 and CD8 markers and move from the cortex to the junction between the cortex and medulla. It is here that negative selection takes place. In negative selection, self-antigens are brought into the thymus from other parts of the body by professional antigen-presenting cells. The T cells that bind to these self-antigens are selected for negatively and are killed by apoptosis. In summary, the only T cells left are those that can bind to MHC molecules of the body with foreign antigens presented on their binding clefts, preventing an attack on one’s own body tissues, at least under normal circumstances. Tolerance can be broken, however, by the development of an autoimmune response, to be discussed later in this chapter.

The cells that leave the thymus become single positives, expressing either CD4 or CD8, but not both (see Figure 4). The CD4+ T cells will bind to class II MHC and the CD8+ cells will bind to class I MHC. The discussion that follows explains the functions of these molecules and how they can be used to differentiate between the different T cell functional types.
Mature T cells become activated by recognizing processed foreign antigen in association with a self-MHC molecule and begin dividing rapidly by mitosis. This proliferation of T cells is called clonal expansion and is necessary to make the immune response strong enough to effectively control a pathogen. How does the body select only those T cells that are needed against a specific pathogen? Again, the specificity of a T cell is based on the amino acid sequence and the three-dimensional shape of the antigen-binding site formed by the variable regions of the two chains of the T cell receptor (Figure 5). Clonal selection is the process of antigen binding only to those T cells that have receptors specific to that antigen. Each T cell that is activated has a specific receptor “hard-wired” into its DNA, and all of its progeny will have identical DNA and T cell receptors, forming clones of the original T cell.
The clonal selection theory was proposed by Frank Burnet in the 1950s. However, the term clonal selection is not a complete description of the theory, as clonal expansion goes hand in glove with the selection process. The main tenet of the theory is that a typical individual has a multitude (1011) of different types of T cell clones based on their receptors. In this use, a clone is a group of lymphocytes that share the same antigen receptor. Each clone is necessarily present in the body in low numbers. Otherwise, the body would not have room for lymphocytes with so many specificities.

Only those clones of lymphocytes whose receptors are activated by the antigen are stimulated to proliferate. Keep in mind that most antigens have multiple antigenic determinants, so a T cell response to a typical antigen involves a polyclonal response. A polyclonal response is the stimulation of multiple T cell clones. Once activated, the selected clones increase in number and make many copies of each cell type, each clone with its unique receptor. By the time this process is complete, the body will have large numbers of specific lymphocytes available to fight the infection (see Figure 5).
As already discussed, one of the major features of an adaptive immune response is the development of immunological memory.

During a primary adaptive immune response, both memory T cells and effector T cells are generated. Memory T cells are long-lived and can even persist for a lifetime. Memory cells are primed to act rapidly. Thus, any subsequent exposure to the pathogen will elicit a very rapid T cell response. This rapid, secondary adaptive response generates large numbers of effector T cells so fast that the pathogen is often overwhelmed before it can cause any symptoms of disease. This is what is meant by immunity to a disease. The same pattern of primary and secondary immune responses occurs in B cells and the antibody response, as will be discussed later in the chapter.
In the discussion of T cell development, you saw that mature T cells express either the CD4 marker or the CD8 marker, but not both. These markers are cell adhesion molecules that keep the T cell in close contact with the antigen-presenting cell by directly binding to the MHC molecule (to a different part of the molecule than does the antigen). Thus, T cells and antigen-presenting cells are held together in two ways: by CD4 or CD8 attaching to MHC and by the T cell receptor binding to antigen (Figure 6).

Although the correlation is not 100 percent, CD4-bearing T cells are associated with helper functions and CD8-bearing T cells are associated with cytotoxicity. These functional distinctions based on CD4 and CD8 markers are useful in defining the function of each type.

A. Helper T Cells and their Cytokines

Helper T cells (Th), bearing the CD4 molecule, function by secreting cytokines that act to enhance other immune responses. There are two classes of Th cells, and they act on different components of the immune response. These cells are not distinguished by their surface molecules but by the characteristic set of cytokines they secrete (Table 2).

Th1 cells are a type of helper T cell that secretes cytokines that regulate the immunological activity and development of a variety of cells, including macrophages and other types of T cells.

Th2 cells, on the other hand, are cytokine-secreting cells that act on B cells to drive their differentiation into plasma cells that make antibody. In fact, T cell help is required for antibody responses to most protein antigens, and these are called T cell-dependent antigens.

B. Cytotoxic T cells

Cytotoxic T cells (Tc) are T cells that kill target cells by inducing apoptosis using the same mechanism as NK cells. They either express Fas ligand, which binds to the fas molecule on the target cell, or act by using perforins and granzymes contained in their cytoplasmic granules. As was discussed earlier with NK cells, killing a virally infected cell before the virus can complete its replication cycle results in the production of no infectious particles. As more Tc cells are developed during an immune response, they overwhelm the ability of the virus to cause disease. In addition, each Tc cell can kill more than one target cell, making them especially effective. Tc cells are so important in the antiviral immune response that some speculate that this was the main reason the adaptive immune response evolved in the first place.

C. Regulatory T Cells

Regulatory T cells (Treg), or suppressor T cells, are the most recently discovered of the types listed here, so less is understood about them. In addition to CD4, they bear the molecules CD25 and FOXP3. Exactly how they function is still under investigation, but it is known that they suppress other T cell immune responses. This is an important feature of the immune response, because if clonal expansion during immune responses were allowed to continue uncontrolled, these responses could lead to autoimmune diseases and other medical issues.

Not only do T cells directly destroy pathogens, but they regulate nearly all other types of the adaptive immune response as well, as evidenced by the functions of the T cell types, their surface markers, the cells they work on, and the types of pathogens they work against (see Table 2).

OpenStax. (2022). Anatomy and Physiology 2e. Rice University. Retrieved June 15, 2023. ISBN-13: 978-1-711494-06-7 (Hardcover) ISBN-13: 978-1-711494-05-0 (Paperback) ISBN-13: 978-1-951693-42-8 (Digital). License: Attribution 4.0 International (CC BY 4.0). Access for free at openstax.org.

Notice the constant and variable regions of each chain, anchored by the transmembrane region.

A typical protein antigen has multiple antigenic determinants, shown by the ability of T cells with three different specificities to bind to different parts of the same antigen.

MHCCell typePhagocytic?Function
Class IManyNoStimulates cytotoxic T cell immune response
Class IIMacrophageYesStimulates phagocytosis and presentation at primary infection site
Class IIDendriticYes, in tissuesBrings antigens to regional lymph nodes
Class IIB cellYes, internalizes surface Ig and antigenStimulates antibody secretion by B cells

Immature T-cells, called thymocytes, enter the thymus and go through a series of developmental stages that ensures both function and tolerance before they leave and become functional components of the adaptive immune response.

Stem cells differentiate into T cells with specific receptors, called clones. The clones with receptors specific for antigens on the pathogen are selected for and expanded.

(a) CD4 is associated with helper and regulatory T cells. An extracellular pathogen is processed and presented in the binding cleft of a class II MHC molecule, and this interaction is strengthened by the CD4 molecule. (b) CD8 is associated with cytotoxic T cells. An intracellular pathogen is presented by a class I MHC molecule, and CD8 interacts with it.

T cellMain targetFunctionPathogenSurface markerMHCCytokines or mediators
TcInfected cellsCytotoxicityIntracellularCD8Class IPerforins, granzymes, and fas ligand
Th1MacrophageHelper inducerExtracellularCD4Class IIInterferon-γ and TGF-β
Th2B cellHelper inducerExtracellularCD4Class IIIL-4, IL-6, IL-10, and others
TregTh cellSuppressorNoneCD4, CD25?TGF-β and IL-10
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Script:
  1. The immune response involves both innate and adaptive components.
  2. While innate responses slow down pathogen growth, the adaptive immune system provides specificity and memory.
  3. The adaptive response recognizes antigens through receptors on B and T lymphocytes, generating a diverse set of receptors through molecular mechanisms.
  4. Upon re-exposure to a pathogen, the secondary adaptive response is faster and stronger due to immunological memory.
  5. The adaptive immune system distinguishes self- from foreign antigens to prevent autoimmune responses.
  6. T cells, particularly important in adaptive immunity, recognize antigens through protein receptors and undergo selection and differentiation processes in the thymus.
  7. Antigen presentation to T cells occurs via major histocompatibility complex (or MHC) molecules, leading to T cell activation and clonal expansion.
  8. Memory T cells ensure rapid responses upon re-exposure to pathogens.
  9. T cells exhibit various functions based on markers like CD4 and CD8.
  10. Helper T cells secrete cytokines to enhance immune responses, cytotoxic T cells kill infected cells, and regulatory T cells suppress immune responses to prevent autoimmune diseases.
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