Animmune response is a physiological reaction which occurs within an organism in the context ofinflammation for the purpose of defending against exogenous factors. These include a wide variety of differenttoxins,viruses, intra- and extracellularbacteria,protozoa,helminths, andfungi which could cause serious problems to the health of the host organism if not cleared from the body.[1]
In addition, there are other forms of immune response. For example, harmless exogenous factors (such as pollen and food components) can triggerallergy; latex and metals are also known allergens.A transplanted tissue (for example, blood) or organ can causegraft-versus-host disease. A type of immune reactivity known asRh disease can be observed in pregnant women. These special forms of immune response are classified ashypersensitivity. Another special form of immune response isantitumor immunity.
In general, there are two branches of the immune response, theinnate and theadaptive, which work together to protect against pathogens. Both branches engagehumoral andcellular components.
The innate branch—the body's first reaction to an invader—is known to be a non-specific and quick response to any sort of pathogen . Components of the innate immune response include physical barriers like the skin and mucous membranes, immune cells such asneutrophils,macrophages, andmonocytes, and soluble factors includingcytokines andcomplement.[2] On the other hand, the adaptive branch is the body's immune response which is catered against specificantigens and thus, it takes longer to activate the components involved. The adaptive branch include cells such asdendritic cells,T cell, andB cells as well asantibodies—also known as immunoglobulins—which directly interact with antigen and are a very important component for a strong response against an invader.[1]
The first contact that an organism has with a particular antigen will result in the production of effector T and B cells which are activated cells that defend against the pathogen. The production of these effector cells as a result of the first-time exposure is called aprimary immune response.Memory T andmemory B cells are also produced in the case that the same pathogen enters the organism again. If the organism does happen to become re-exposed to the same pathogen, asecondary immune response will kick in and the immune system will be able to respond in both a fast and strong manner because of the memory cells from the first exposure.[3]Vaccines introduce a weakened, killed, or fragmented microorganism in order to evoke a primary immune response. This is so that in the case that an exposure to the real pathogen occurs, the body can rely on the secondary immune response to quickly defend against it.[4]

Theinnate immune response is an organism's first response to foreign invaders. This immune response is evolutionarily conserved across many different species, with all multi-cellular organisms having some sort of variation of an innate response.[5] The innate immune system consists of physical barriers such asskin andmucous membranes, various cell types likeneutrophils,macrophages, andmonocytes, and soluble factors includingcytokines and complement.[2] In contrast to theadaptive immune response, the innate response is not specific to any one foreign invader and as a result, works quickly to rid the body of pathogens.[citation needed]
Pathogens are recognized and detected viapattern recognition receptors (PRR). These receptors are structures on the surface of macrophages which are capable of binding foreign invaders and thus initiatingcell signaling within the immune cell. Specifically, the PRRs identifypathogen-associated molecular patterns (PAMPs) which are integral structural components of pathogens. Examples of PAMPs include thepeptidoglycan cell wall orlipopolysaccharides (LPS), both of which are essential components of bacteria and are therefore evolutionarily conserved across many different bacterial species.[6]
When a foreign pathogen bypasses the physical barriers and enters an organism, the PRRs on macrophages will recognize and bind to specific PAMPs. This binding results in the activation of asignaling pathway which allows for thetranscription factorNF-κB to enter the nucleus of the macrophage and initiate the transcription and eventual secretion of variouscytokines such asIL-8,IL-1, andTNFα.[5] Release of these cytokines is necessary for the entry ofneutrophils from theblood vessels to the infected tissue. Once neutrophils enter the tissue, like macrophages, they are able tophagocytize and kill any pathogens or microbes.[citation needed]
Complement, another component of the innate immune system, consists of three pathways that are activated in distinct ways. The classical pathway is triggered when IgG or IgM is bound to its target antigen on either the pathogen cell membrane or an antigen-bound antibody. The alternative pathway is activated by foreign surfaces such as viruses, fungi, bacteria, parasites, etc., and is capable of autoactivation due to “tickover” of C3. Thelectin pathway is triggered whenmannose-binding lectin (MBL) orficolin aka specific pattern recognition receptors bind to pathogen-associated molecular patterns on the surface of invading microorganisms such asyeast, bacteria, parasites, and viruses.[7] Each of the three pathways ensures that complement will still be functional if one pathway ceases to work or a foreign invader is able to evade one of these pathways (defense in depth principle).[5] Though the pathways are activated differently, the overall role of the complement system is toopsonize pathogens and induce a series ofinflammatory responses that help to combatinfection.[citation needed]

Theadaptive immune response is the body'ssecond line of defense. The cells of the adaptive immune system are extremely specific because during early developmental stages the B and T cells develop antigen receptors that are specific to only certainantigens. This is extremely important for B and T cell activation. B and T cells are extremely dangerous cells, and if they are able to attack without undergoing a rigorous process of activation, a faulty B or T cell can begin exterminating the host's own healthy cells.[8] Activation of naïve helper T cells occurs whenantigen-presenting cells (APCs) present foreign antigen viaMHC class II molecules on their cell surface. These APCs includedendritic cells,B cells, andmacrophages which are specially equipped not only with MHC class II but also with co-stimulatory ligands which are recognized by co-stimulatory receptors on helper T cells. Without the co-stimulatory molecules, the adaptive immune response would be inefficient and T cells would becomeanergic. Several T cell subgroups can be activated by specific APCs, and each T cell is specially equipped to deal with each unique microbial pathogen. The type of T cell activated and the type of response generated depends, in part, on the context in which the APC first encountered the antigen.[9] Once helper T cells are activated, they are able to activate naïve B cells in thelymph node. However, B cell activation is a two-step process. Firstly, B cell receptors, which are justImmunoglobulin M (IgM) andImmunoglobulin D (IgD) antibodies specific to the particular B cell, must bind to the antigen which then results in internal processing so that it is presented on the MHC class II molecules of the B cell. Once this happens a T helper cell which is able to identify the antigen bound to the MHC interacts with its co-stimulatory molecule and activates the B cell. As a result, the B cell becomes aplasma cell which secretes antibodies that act as anopsonin against invaders.[citation needed]
Specificity in the adaptive branch is due to the fact that every B and T cell is different. Thus there is a diverse community of cells ready to recognize and attack a full range of invaders.[8] The trade-off, however, is that the adaptive immune response is much slower than the body's innate response because its cells are extremely specific and activation is required before it is able to actually act. In addition to specificity, the adaptive immune response is also known forimmunological memory. After encountering an antigen, the immune system produces memory T and B cells which allow for a speedier, more robust immune response in the case that the organism ever encounters the same antigen again.[8]

Depending on exogenous demands, several types of immune response (IR) are distinguished. In this paradigm, immune system (both innate and adaptive) and non-immune system cellular and molecular components are organized to optimally respond to distinct exposome challenges.
Currently, several types of IR are classified.[10][11]
Type 1 IR is elicited by viruses, intracellular bacteria, parasites. The actors here are group 1innate lymphoid cells (ILC1), NK cells, Th1 cells, macrophages, opsonizing IgG isotypes.
Type 2 IR is caused bytoxins and multicellular parasites. ILC2,epithelial cells, Th2 lymphocytes, eosinophils, basophils, mast cells, IgE are key players here.
Type 3 IR targets extracellular bacteria and fungi by recruiting ILC3, Th17, neutrophils, opsonizing IgG isotypes.
Additional types of IR can be observed in noninfectious pathologies.[12]
All types of IR havesensor (ILCs, NK cells),adaptive (T and B cells), andeffector (neutrophils,eosinophils,basophils,mast cells) parts.[11]
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