Innate immune system

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Innate immune system

The innate immune system or nonspecific immune system

fungi, prokaryotes, and invertebrates (see Beyond vertebrates).[2]

The major functions of the innate immune system are to:

Anatomical barriers

Anatomical barriers include physical, chemical and biological barriers. The epithelial surfaces form a physical barrier that is impermeable to most infectious agents, acting as the first line of defense against invading organisms.

Gut flora can prevent the colonization of pathogenic bacteria by secreting toxic substances or by competing with pathogenic bacteria for nutrients or cell surface attachment sites.[3] The flushing action of tears and saliva helps prevent infection of the eyes and mouth.[3]

Anatomical barrier Additional defense mechanisms
Skin Sweat (including
cathelicidin, desquamation, flushing,[3] organic acids,[3] skin flora
Gastrointestinal tract
gut flora,[3] lysozymes
lungs
 Mucociliary escalator,
defensins[3]
Nasopharynx
 Mucus, saliva, lysozyme[3]
Eyes Tears[3]
Blood–brain barrier
endothelial cells (via passive diffusion/ osmosis & active selection). P-glycoprotein (mechanism by which active transportation
is mediated)

Inflammation

Main article: Inflammation

Inflammation is one of the first responses of the immune system to infection or irritation. Inflammation is stimulated by chemical factors released by injured cells. It establishes a physical barrier against the spread of infection and promotes healing of any damaged tissue following pathogen clearance.[5]

The process of acute inflammation is initiated by cells already present in all tissues, mainly resident

inflammatory mediators, like cytokines and chemokines, which are responsible for the clinical signs of inflammation. PRR activation and its cellular consequences have been well-characterized as methods of inflammatory cell death, which include pyroptosis, necroptosis, and PANoptosis
. These cell death pathways help clear infected or aberrant cells and release cellular contents and inflammatory mediators.

Chemical factors produced during inflammation (

IL-1.[6]

The inflammatory response is characterized by the following symptoms:

  • redness of the skin, due to locally increased blood circulation;
  • heat, either increased local temperature, such as a warm feeling around a localized infection, or a systemic fever;
  • swelling of affected tissues, such as the upper throat during the common cold or joints affected by rheumatoid arthritis;
  • increased production of mucus, which can cause symptoms like a
    productive cough
    ;
  • pain, either local pain, such as
    body aches
    ; and
  • possible dysfunction of involved organs/tissues.

Complement system

Main article: Complement system

The

hepatocytes
. The proteins work together to:

  • trigger the recruitment of inflammatory cells
  • "tag" pathogens for destruction by other cells by opsonizing, or coating, the surface of the pathogen
  • form holes in the plasma membrane of the pathogen, resulting in cytolysis of the pathogen cell, causing its death
  • rid the body of neutralised antigen-antibody complexes.

The three different complement systems are classical, alternative and lectin.

  • Classical: starts when antibody binds to bacteria
  • Alternative: starts "spontaneously"
  • Lectin: starts when lectins bind to mannose on bacteria

Elements of the complement cascade can be found in many non-mammalian species including plants, birds, fish, and some species of invertebrates.[7]

White blood cells

Main article:
Leukocyte
See also: Cells of the innate immune system
A scanning electron microscope image of normal circulating human blood. One can see red blood cells, several knobby white blood cells including lymphocytes, a monocyte, a neutrophil, and many small disc-shape platelets.

White blood cells (WBCs) are also known as

leukocytes. Most leukocytes differ from other cells of the body in that they are not tightly associated with a particular organ or tissue; thus, their function is similar to that of independent, single-cell organisms. Most leukocytes are able to move freely and interact with and capture cellular debris, foreign particles, and invading microorganisms (although macrophages, mast cells, and dendritic cells are less mobile). Unlike many other cells, most innate immune leukocytes cannot divide or reproduce on their own, but are the products of multipotent hematopoietic stem cells present in bone marrow.[8][9]

The innate leukocytes include:

neutrophils, and dendritic cells, and function within the immune system by identifying and eliminating pathogens that might cause infection.[2]

Mast cells

Main article: Mast cell

Mast cells are a type of innate immune cell that resides in connective tissue and in mucous membranes. They are intimately associated with wound healing and defense against pathogens, but are also often associated with allergy and anaphylaxis.[5] When activated, mast cells rapidly release characteristic granules, rich in histamine and heparin, along with various hormonal mediators and chemokines, or chemotactic cytokines into the environment. Histamine dilates blood vessels, causing the characteristic signs of inflammation, and recruits neutrophils and macrophages.[5]

Phagocytes

Main article: Phagocyte

The word 'phagocyte' literally means 'eating cell'. These are immune cells that engulf, or '

neutrophils
, and dendritic cells.

Phagocytosis of the hosts' own cells is common as part of regular tissue development and maintenance. When host cells die, either by apoptosis or by cell injury due to an infection, phagocytic cells are responsible for their removal from the affected site.[9] By helping to remove dead cells preceding growth and development of new healthy cells, phagocytosis is an important part of the healing process following tissue injury.

A macrophage

Macrophages

Main article:
Macrophages

Macrophages, from the Greek, meaning "large eaters", are large phagocytic leukocytes, which are able to move beyond the vascular system by migrating through the walls of capillary vessels and entering the areas between cells in pursuit of invading pathogens. In tissues, organ-specific macrophages are differentiated from phagocytic cells present in the blood called monocytes. Macrophages are the most efficient phagocytes and can phagocytose substantial numbers of bacteria or other cells or microbes.[2] The binding of bacterial molecules to receptors on the surface of a macrophage triggers it to engulf and destroy the bacteria through the generation of a "respiratory burst", causing the release of reactive oxygen species. Pathogens also stimulate the macrophage to produce chemokines, which summon other cells to the site of infection.[2]

Neutrophils

Main article:
Neutrophils
A neutrophil

Neutrophils, along with

acute inflammation.[5]

Dendritic cells

Main article: Dendritic cell

Dendritic cells (DCs) are phagocytic cells present in tissues that are in contact with the external environment, mainly the

neuronal dendrites, but dendritic cells are not connected to the nervous system. Dendritic cells are very important in the process of antigen presentation, and serve as a link between the innate and adaptive immune systems
.

An eosinophil

Basophils and eosinophils

Main articles:
Eosinophil granulocyte

Basophils and eosinophils are cells related to the neutrophil. When activated by a pathogen encounter,

toxic proteins and free radicals that are highly effective in killing parasites, but may also damage tissue during an allergic reaction. Activation and release of toxins by eosinophils are, therefore, tightly regulated to prevent any inappropriate tissue destruction.[5]

Natural killer cells

Main article: Natural killer cell

immunoglobulin receptors (KIR) that slow the reaction of NK cells. The NK-92 cell line does not express KIR and is developed for tumor therapy.[11][12][13][14]

γδ T cells

Main article:
gamma/delta T cells

Like other 'unconventional' T cell subsets bearing invariant

Natural Killer T cells, γδ T cells exhibit characteristics that place them at the border between innate and adaptive immunity. γδ T cells may be considered a component of adaptive immunity in that they rearrange TCR genes to produce junctional diversity and develop a memory phenotype. The various subsets may be considered part of the innate immune system where a restricted TCR or NK receptors may be used as a pattern recognition receptor. For example, according to this paradigm, large numbers of Vγ9/Vδ2 T cells respond within hours to common molecules
produced by microbes, and highly restricted intraepithelial Vδ1 T cells will respond to stressed epithelial cells.

Other vertebrate mechanisms

The

beta-lysine, a protein produced by platelets during coagulation, can cause lysis of many Gram-positive bacteria by acting as a cationic detergent.[3] Many acute-phase proteins of inflammation
are involved in the coagulation system.

Increased levels of lactoferrin and transferrin inhibit bacterial growth by binding iron, an essential bacterial nutrient.[3]

Neural regulation

The innate immune response to infectious and sterile injury is modulated by neural circuits that control cytokine production period. The inflammatory reflex is a prototypical neural circuit that controls cytokine production in the spleen.[15] Action potentials transmitted via the vagus nerve to the spleen mediate the release of acetylcholine, the neurotransmitter that inhibits cytokine release by interacting with alpha7 nicotinic acetylcholine receptors (CHRNA7) expressed on cytokine-producing cells.[16] The motor arc of the inflammatory reflex is termed the cholinergic anti-inflammatory pathway.

Pathogen-specificity

The parts of the innate immune system display specificity for different pathogens.

Pathogen Main examples[17] Phagocytosis[17] complement[17]
NK cells[17]
Intracellular and cytoplasmic virus yes yes[18] yes
Intracellular bacteria yes (specifically
neutrophils
)		 yes[19] yes
no yes yes
Extracellular bacteria yes yes no
Intracellular protozoa no no yes
Extracellular protozoa yes yes no/yes
Extracellular
fungi
 no yes yes[20]

Immune evasion

Innate immune system cells prevent free growth of microorganisms within the body, but many pathogens have evolved mechanisms to evade it.[21][22]

One strategy is intracellular replication, as practised by

B. fragilis are opportunistic pathogens, causing infections of the peritoneal cavity. They inhibit phagocytosis by affecting the phagocytes receptors used to engulf bacteria. They may also mimic host cells so the immune system does not recognize them as foreign. Staphylococcus aureus inhibits the ability of the phagocyte to respond to chemokine signals. M. tuberculosis, Streptococcus pyogenes, and Bacillus anthracis utilize mechanisms that directly kill the phagocyte.[citation needed
]

Bacteria and fungi may form complex biofilms, protecting them from immune cells and proteins; biofilms are present in the chronic Pseudomonas aeruginosa and Burkholderia cenocepacia infections characteristic of cystic fibrosis.[25]

Viruses

Type I

antiviral protein production, such as protein kinase R, which inhibits viral protein synthesis, or the 2′,5′-oligoadenylate synthetase family, which degrades viral RNA.[27]

Some viruses evade this by producing molecules that interfere with IFN production. For example, the

Influenza A virus produces NS1 protein, which can bind to host and viral RNA, interact with immune signaling proteins or block their activation by ubiquitination, thus inhibiting type I IFN production.[29] Influenza A also blocks protein kinase R activation and establishment of the antiviral state.[30] The dengue virus also inhibits type I IFN production by blocking IRF-3 phosophorylation using NS2B3 protease complex.[31]

Beyond vertebrates

Prokaryotes

restriction endonucleases, that attack and destroy specific regions of the viral DNA of invading bacteriophages. Methylation of the host's own DNA marks it as "self" and prevents it from being attacked by endonucleases.[32] Restriction endonucleases and the restriction modification system exist exclusively in prokaryotes.[33]

Invertebrates

coelomates (animals with a body-cavity), including humans.[35] The complement system exists in most life forms. Some invertebrates, including various insects, crabs, and worms utilize a modified form of the complement response known as the prophenoloxidase (proPO) system.[34]

immunity. Several species of insect produce antimicrobial peptides known as defensins and cecropins
.

Proteolytic cascades

In invertebrates, PRRs trigger proteolytic cascades that degrade proteins and control many of the mechanisms of the innate immune system of invertebrates—including hemolymph coagulation and melanization. Proteolytic cascades are important components of the invertebrate immune system because they are turned on more rapidly than other innate immune reactions because they do not rely on gene changes. Proteolytic cascades function in both vertebrate and invertebrates, even though different proteins are used throughout the cascades.[36]

Clotting mechanisms

In the hemolymph, which makes up the fluid in the circulatory system of

lipopolysaccharides enter.[36]

Plants

Main article: Plant disease resistance § Immune system

Members of every class of pathogen that infect humans also infect plants. Although the exact pathogenic species vary with the infected species, bacteria, fungi, viruses, nematodes, and insects can all cause

metabolic responses that lead to the formation of defensive chemical compounds that fight infection or make the plant less attractive to insects and other herbivores.[37] (see: plant defense against herbivory
).

Like invertebrates, plants neither generate antibody or T-cell responses nor possess mobile cells that detect and attack pathogens. In addition, in case of infection, parts of some plants are treated as disposable and replaceable, in ways that few animals can. Walling off or discarding a part of a plant helps stop infection spread.[37]

Most plant immune responses involve systemic chemical signals sent throughout a plant. Plants use PRRs to recognize conserved microbial signatures. This recognition triggers an immune response. The first plant receptors of conserved microbial signatures were identified in rice (

elicitors, the plant produces a localized hypersensitive response (HR), in which cells at the site of infection undergo rapid apoptosis to prevent spread to other parts of the plant. HR has some similarities to animal pyroptosis, such as a requirement of caspase-1-like proteolytic activity of VPEγ, a cysteine protease that regulates cell disassembly during cell death.[41]

"Resistance" (R) proteins, encoded by

jasmonates in transmission of the signal to distal portions of the plant. RNA silencing mechanisms are important in the plant systemic response, as they can block virus replication.[44] The jasmonic acid response is stimulated in leaves damaged by insects, and involves the production of methyl jasmonate.[37]

See also

References

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External links

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