Module 6: The Lymphatic and Immune Systems

Lesson 2: The Innate Immune Response

Đáp Ứng Miễn Dịch Bẩm Sinh

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Dưới đây là danh sách những thuật ngữ Y khoa của module The Lymphatic and Immune Systems.
Khái quát được số lượng thuật ngữ sẽ xuất hiện trong bài đọc và nghe sẽ giúp bạn thoải mái tiêu thụ nội dung hơn. Sau khi hoàn thành nội dung đọc và nghe, bạn hãy quay lại đây và luyện tập (practice) để quen dần các thuật ngữ này. Đừng ép bản thân phải nhớ các thuật ngữ này vội vì bạn sẽ gặp và ôn lại danh sách này trong những bài học (lesson) khác của cùng một module.

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
Nội dung này đang được cập nhật.
Dưới đây là các bài văn nằm ở bên trái. Ở bên phải là các bài luyện tập (practice) để đánh giá khả năng đọc hiểu của bạn. Sẽ khó khăn trong thời gian đầu nếu vốn từ vựng của bạn còn hạn chế, đặc biệt là từ vựng Y khoa. Hãy kiên nhẫn và đọc nhiều nhất có kể, lượng kiến thức tích tụ dần sẽ giúp bạn đọc thoải mái hơn.
The immune system can be divided into two overlapping mechanisms to destroy pathogens: the innate immune response, which is relatively rapid but nonspecific and thus not always effective, and the adaptive immune response, which is slower in its development during an initial infection with a pathogen, but is highly specific and effective at attacking a wide variety of pathogens (Figure 1).
Any discussion of the innate immune response usually begins with the physical barriers that prevent pathogens from entering the body, destroy them after they enter, or flush them out before they can establish themselves in the hospitable environment of the body’s soft tissues. Barrier defenses are part of the body’s most basic defense mechanisms. The barrier defenses are not a response to infections, but they are continuously working to protect against a broad range of pathogens.

The different modes of barrier defenses are associated with the external surfaces of the body, where pathogens may try to enter (Table 1). The primary barrier to the entrance of microorganisms into the body is the skin. Not only is the skin covered with a layer of dead, keratinized epithelium that is too dry for bacteria in which to grow, but as these cells are continuously sloughed off from the skin, they carry bacteria and other pathogens with them. Additionally, sweat and other skin secretions may lower pH, contain toxic lipids, and physically wash microbes away.

Another barrier is the saliva in the mouth, which is rich in lysozyme—an enzyme that destroys bacteria by digesting their cell walls. The acidic environment of the stomach, which is fatal to many pathogens, is also a barrier. Additionally, the mucus layer of the gastrointestinal tract, respiratory tract, reproductive tract, eyes, ears, and nose traps both microbes and debris, and facilitates their removal. In the case of the upper respiratory tract, ciliated epithelial cells move potentially contaminated mucus upwards to the mouth, where it is then swallowed into the digestive tract, ending up in the harsh acidic environment of the stomach. Considering how often you breathe compared to how often you eat or perform other activities that expose you to pathogens, it is not surprising that multiple barrier mechanisms have evolved to work in concert to protect this vital area.
A phagocyte is a cell that is able to surround and engulf a particle or cell, a process called phagocytosis. The phagocytes of the immune system engulf other particles or cells, either to clean an area of debris, old cells, or to kill pathogenic organisms such as bacteria. The phagocytes are the body’s fast acting, first line of immunological defense against organisms that have breached barrier defenses and have entered the vulnerable tissues of the body.

A. Phagocytes: Macrophages and Neutrophils

Many of the cells of the immune system have a phagocytic ability, at least at some point during their life cycles. Phagocytosis is an important and effective mechanism of destroying pathogens during innate immune responses. The phagocyte takes the organism inside itself as a phagosome, which subsequently fuses with a lysosome and its digestive enzymes, effectively killing many pathogens. On the other hand, some bacteria including Mycobacteria tuberculosis, the cause of tuberculosis, may be resistant to these enzymes and are therefore much more difficult to clear from the body. Macrophages, neutrophils, and dendritic cells are the major phagocytes of the immune system.

A macrophage is an irregularly shaped phagocyte that is amoeboid in nature and is the most versatile of the phagocytes in the body. Macrophages move through tissues and squeeze through capillary walls using pseudopodia. They not only participate in innate immune responses but have also evolved to cooperate with lymphocytes as part of the adaptive immune response. Macrophages exist in many tissues of the body, either freely roaming through connective tissues or fixed to reticular fibers within specific tissues such as lymph nodes. When pathogens breach the body’s barrier defenses, macrophages are the first line of defense (Table 2). They are called different names, depending on the tissue: Kupffer cells in the liver, histiocytes in connective tissue, and alveolar macrophages in the lungs.

A neutrophil is a phagocytic cell that is attracted via chemotaxis from the bloodstream to infected tissues. These spherical cells are granulocytes. A granulocyte contains cytoplasmic granules, which in turn contain a variety of vasoactive mediators such as histamine. In contrast, macrophages are agranulocytes. An agranulocyte has few or no cytoplasmic granules. Whereas macrophages act like sentries, always on guard against infection, neutrophils can be thought of as military reinforcements that are called into a battle to hasten the destruction of the enemy. Although, usually thought of as the primary pathogen-killing cell of the inflammatory process of the innate immune response, new research has suggested that neutrophils play a role in the adaptive immune response as well, just as macrophages do.

A monocyte is a circulating precursor cell that differentiates into either a macrophage or dendritic cell, which can be rapidly attracted to areas of infection by signal molecules of inflammation.

B. Natural Killer Cells

NK cells are a type of lymphocyte that have the ability to induce apoptosis, that is, programmed cell death, in cells infected with intracellular pathogens such as obligate intracellular bacteria and viruses. NK cells recognize these cells by mechanisms that are still not well understood, but that presumably involve their surface receptors. NK cells can induce apoptosis, in which a cascade of events inside the cell causes its own death by either of two mechanisms:

  1. NK cells are able to respond to chemical signals and express the fas ligand. The fas ligand is a surface molecule that binds to the fas molecule on the surface of the infected cell, sending it apoptotic signals, thus killing the cell and the pathogen within it; or
  2. The granules of the NK cells release perforins and granzymes. A perforin is a protein that forms pores in the membranes of infected cells. A granzyme is a protein-digesting enzyme that enters the cell via the perforin pores and triggers apoptosis intracellularly.

Both mechanisms are especially effective against virally infected cells. If apoptosis is induced before the virus has the ability to synthesize and assemble all its components, no infectious virus will be released from the cell, thus preventing further infection.
Cells of the innate immune response, the phagocytic cells, and the cytotoxic NK cells recognize patterns of pathogen-specific molecules, such as bacterial cell wall components or bacterial flagellar proteins, using pattern recognition receptors. A pattern recognition receptor (PRR) is a membrane-bound receptor that recognizes characteristic features of a pathogen and molecules released by stressed or damaged cells.

These receptors, which are thought to have evolved prior to the adaptive immune response, are present on the cell surface whether they are needed or not. Their variety, however, is limited by two factors. First, the fact that each receptor type must be encoded by a specific gene requires the cell to allocate most or all of its DNA to make receptors able to recognize all pathogens. Secondly, the variety of receptors is limited by the finite surface area of the cell membrane. Thus, the innate immune system must “get by” using only a limited number of receptors that are active against as wide a variety of pathogens as possible. This strategy is in stark contrast to the approach used by the adaptive immune system, which uses large numbers of different receptors, each highly specific to a particular pathogen.

Should the cells of the innate immune system come into contact with a species of pathogen they recognize, the cell will bind to the pathogen and initiate phagocytosis (or cellular apoptosis in the case of an intracellular pathogen) in an effort to destroy the offending microbe. Receptors vary somewhat according to cell type, but they usually include receptors for bacterial components and for complement, discussed below.
The previous discussions have alluded to chemical signals that can induce cells to change various physiological characteristics, such as the expression of a particular receptor. These soluble factors are secreted during innate or early induced responses, and later during adaptive immune responses.

A. Cytokines and Chemokines

A cytokine is signaling molecule that allows cells to communicate with each other over short distances. Cytokines are secreted into the intercellular space, and the action of the cytokine induces the receiving cell to change its physiology. A chemokine is a soluble chemical mediator similar to cytokines except that its function is to attract cells (chemotaxis) from longer distances.

B. Early induced Proteins

Early induced proteins are those that are not constitutively present in the body, but are made as they are needed early during the innate immune response. Interferons are an example of early induced proteins. Cells infected with viruses secrete interferons that travel to adjacent cells and induce them to make antiviral proteins. Thus, even though the initial cell is sacrificed, the surrounding cells are protected. Other early induced proteins specific for bacterial cell wall components are mannose-binding protein and C-reactive protein, made in the liver, which bind specifically to polysaccharide components of the bacterial cell wall. Phagocytes such as macrophages have receptors for these proteins, and they are thus able to recognize them as they are bound to the bacteria. This brings the phagocyte and bacterium into close proximity and enhances the phagocytosis of the bacterium by the process known as opsonization. Opsonization is the tagging of a pathogen for phagocytosis by the binding of an antibody or an antimicrobial protein.

C. Complement System

The complement system is a series of proteins constitutively found in the blood plasma. As such, these proteins are not considered part of the early induced immune response, even though they share features with some of the antibacterial proteins of this class. Made in the liver, they have a variety of functions in the innate immune response, using what is known as the “alternate pathway” of complement activation. Additionally, complement functions in the adaptive immune response as well, in what is called the classical pathway. The complement system consists of several proteins that enzymatically alter and fragment later proteins in a series, which is why it is termed cascade. Once activated, the series of reactions is irreversible, and releases fragments that have the following actions:

  • Bind to the cell membrane of the pathogen that activates it, labeling it for phagocytosis (opsonization.)
  • Diffuse away from the pathogen and act as chemotactic agents to attract phagocytic cells to the site of inflammation.
  • Form damaging pores in the plasma membrane of the pathogen.

Figure 2 shows the classical pathway, which requires antibodies of the adaptive immune response. The alternate pathway does not require an antibody to become activated.

The splitting of the C3 protein is the common step to both pathways. In the alternate pathway, C3 is activated spontaneously and, after reacting with the molecules factor P, factor B, and factor D, splits apart. The larger fragment, C3b, binds to the surface of the pathogen and C3a, the smaller fragment, diffuses outward from the site of activation and attracts phagocytes to the site of infection. Surface-bound C3b then activates the rest of the cascade, with the last five proteins, C5–C9, forming the membrane-attack complex (MAC). The MAC can kill certain pathogens by disrupting their osmotic balance. The MAC is especially effective against a broad range of bacteria. The classical pathway is similar, except the early stages of activation require the presence of antibody bound to antigen, and thus is dependent on the adaptive immune response. The earlier fragments of the cascade also have important functions. Phagocytic cells such as macrophages and neutrophils are attracted to an infection site by chemotactic attraction to smaller complement fragments. Additionally, once they arrive, their receptors for surface-bound C3b opsonize the pathogen for phagocytosis and destruction.
The hallmark of the innate immune response is inflammation. Inflammation is something everyone has experienced. Stub a toe, cut a finger, or do any activity that causes tissue damage and inflammation will result, with its four characteristics: heat, redness, pain, and swelling (“loss of function” is sometimes mentioned as a fifth characteristic). It is important to note that inflammation does not have to be initiated by an infection, but can also be caused by tissue injuries. The release of damaged cellular contents into the site of injury is enough to stimulate the response, even in the absence of breaks in physical barriers that would allow pathogens to enter (by hitting your thumb with a hammer, for example). The inflammatory reaction brings in phagocytic cells to the damaged area to clear cellular debris and to set the stage for wound repair (Figure 3).

This reaction also brings in the cells of the innate immune system, allowing them to get rid of the sources of a possible infection. Inflammation is part of a very basic form of immune response. The process not only brings fluid and cells into the site to destroy the pathogen and remove it and debris from the site, but also helps to isolate the site, limiting the spread of the pathogen. Acute inflammation is a short-term inflammatory response to an insult to the body. If the cause of the inflammation is not resolved, however, it can lead to chronic inflammation, which is associated with major tissue destruction and fibrosis. Chronic inflammation is ongoing inflammation. It can be caused by foreign bodies, persistent pathogens, and autoimmune diseases such as rheumatoid arthritis.

There are four important parts to the inflammatory response:

  1. Tissue Injury. The released contents of injured cells stimulate the release of mast cell granules and their potent inflammatory mediators such as histamine, leukotrienes, and prostaglandins. Histamine increases the diameter of local blood vessels (vasodilation), causing an increase in blood flow. Histamine also increases the permeability of local capillaries, causing plasma to leak out and form interstitial fluid. This causes the swelling associated with inflammation.
    Additionally, injured cells, phagocytes, and basophils are sources of inflammatory mediators, including prostaglandins and leukotrienes. Leukotrienes attract neutrophils from the blood by chemotaxis and increase vascular permeability. Prostaglandins cause vasodilation by relaxing vascular smooth muscle and are a major cause of the pain associated with inflammation. Nonsteroidal anti-inflammatory drugs such as aspirin and ibuprofen relieve pain by inhibiting prostaglandin production.
  2. Vasodilation. Many inflammatory mediators such as histamine are vasodilators that increase the diameters of local capillaries. This causes increased blood flow and is responsible for the heat and redness of inflamed tissue. It allows greater access of the blood to the site of inflammation.
  3. Increased Vascular Permeability. At the same time, inflammatory mediators increase the permeability of the local vasculature, causing leakage of fluid into the interstitial space, resulting in the swelling, or edema, associated with inflammation.
  4. Recruitment of Phagocytes. Leukotrienes are particularly good at attracting neutrophils from the blood to the site of infection by chemotaxis. Following an early neutrophil infiltrate stimulated by macrophage cytokines, more macrophages are recruited to clean up the debris left over at the site. When local infections are severe, neutrophils are attracted to the sites of infections in large numbers, and as they phagocytose the pathogens and subsequently die, their accumulated cellular remains are visible as pus at the infection site.

Overall, inflammation is valuable for many reasons. Not only are the pathogens killed and debris removed, but the increase in vascular permeability encourages the entry of clotting factors, the first step towards wound repair. Inflammation also facilitates the transport of antigen to lymph nodes by dendritic cells for the development of the adaptive immune response.

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.

The innate immune system enhances adaptive immune responses so they can be more effective.

SiteSpecific defenseProtective aspect
SkinEpidermal surfaceKeratinized cells of surface, Langerhans cells
Skin (sweat/secretions)Sweat glands, sebaceous glandsLow pH, washing action
Oral cavitySalivary glandsLysozyme
StomachGastrointestinal tractLow pH
Mucosal surfacesMucosal epitheliumNonkeratinized epithelial cells
Normal flora (nonpathogenic bacteria)Mucosal tissuesPrevent pathogens from growing on mucosal surfaces
CellCell typePrimary locationFunction in the innate immune response
MacrophageAgranulocyteBody cavities/organsPhagocytosis
NeutrophilGranulocyteBloodPhagocytosis
MonocyteAgranulocyteBloodPrecursor of macrophage/dendritic cell

The classical pathway, used during adaptive immune responses, occurs when C1 reacts with antibodies that have bound an antigen.

The top panel of this figure shows the mast cells detecting an injury and initiating an inflammatory response. The bottom panel shows the increase in blood flow in response to histamine.

Events resulting in warmth, redness, pain, and swelling, as well as the recruitment of phagocytes.

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Script:
  1. The immune system comprises two main mechanisms for combating pathogens: the innate immune response and the adaptive immune response.
  2. The innate immune response acts as the body’s first line of defense against pathogens, employing nonspecific but rapid mechanisms to prevent entry, destroy, or flush out invaders.
  3. Physical barriers like the skin, saliva, stomach acidity, mucus, and ciliated epithelial cells in the respiratory tract form crucial components of innate immunity, constantly working to thwart pathogens from gaining access to the body’s soft tissues.
  4. These barrier defenses provide a formidable shield against a wide array of pathogens and are complemented by cellular components of the innate immune system.
  5. Phagocytes, including macrophages and neutrophils, are key players in the innate immune response, swiftly engulfing and neutralizing pathogens through phagocytosis.
  6. Macrophages, versatile and widely distributed throughout the body, act as sentinels, detecting and eliminating pathogens in various tissues.
  7. Neutrophils, mobilized from the bloodstream to infected tissues, serve as rapid reinforcements, aiding in the destruction of pathogens.
  8. Additionally, natural killer cells, a type of lymphocyte, induce apoptosis in infected cells, particularly those harboring intracellular pathogens like viruses and certain bacteria.
  9. Recognition of pathogens by cells of the innate immune system relies on pattern recognition receptors (or PRRs), which identify characteristic features of pathogens or stressed cells.
  10. This recognition triggers phagocytosis or apoptosis, initiating the immune response.
  11. Soluble mediators such as cytokines, chemokines, and early induced proteins play crucial roles in coordinating immune responses, regulating cell functions, and attracting immune cells to sites of infection.
  12. The complement system, consisting of plasma proteins, enhances the innate immune response by opsonizing pathogens for phagocytosis, inducing inflammation, and forming membrane attack complexes to kill certain pathogens directly.
  13. Inflammation, characterized by heat, redness, pain, and swelling, is a hallmark of innate immunity, facilitating pathogen clearance, tissue repair, and the initiation of adaptive immune responses.
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