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Macrophages consume antigens, and present their shape on the surface. T cells attach to these antigens to create T Helper cells, so antibodies can be created by B cells, Effector B cells, Memory B cells, and Killer T cells can rid all infected cells

The Immune response is the body's response caused by its immune system being activated by antigens. The immune response can include immunity to pathogenic microorganisms and its products, allergies, graft rejections, as well as autoimmunity to self-antigens. In this process the main cells involved are T cells and B cells (sub-types of lymphocytes), and macrophages (a type of leucocyte or white blood cell). These cells produce lymphokines that influence the other host cells' activities. B cells, when activated by helper T cells undergo clonal expansion. B cells differentiate into plasma cells, which are short lived and secrete antibodies, and memory B cells, which are long lived and produce a fast, remembered response when exposed to the same infection in the future. B cells mature to produce immunoglobulins (also known as antibodies), that react with antigens. At the same time, macrophages process the antigens into immunogenic units which stimulate B lymphocytes to differentiate into antibody-secreting plasma cells, stimulating the T cells to release lymphokines.[1]

Complement is a group of normal serum proteins that enhance the immune response by becoming activated as the result of antigen-antibody interaction. The first contact with any antigen sensitize individual affected and promote the primary immune response. Next of the sensitized individuals with same antigen result in a more rapid and massive reaction, called the secondary immune response ("booster response" or the "anamnestic reaction"). It is most expressed in the level of circulating serum antibodies.[2][3]

An anamnestic response in medicine is a delayed immunologic response. The term is frequently used in transfusion medicine and refers to a re-exposure incident where antibody is formed on initial exposure to an antigen in a transfused unit, but the specific memory B cell population fades over time, with antibody becoming undetectable over years. If a patient is re-exposed to the same offending antigen in a future transfusion (which might happen because the antibody screen would in fact be negative), there would still be a massive, rapid production of IgG antibody against the antigen, which will predictably lyse the transfused red cells, a delayed hemolytic transfusion reaction.[citation needed]

Drawing of a primary immune response with B-cells and T-cells

The immune response can be transferred via serum antibodies introduction from sensitized to desensitized individuals. It is highly specific for given antigen, and it is normally directed against foreign protein substances.[2]



Innate response is the first line of defense when it comes to defending an organism from an foreign invader. Foreign invaders include bacteria, viruses, and parasites. The protection an innate response offers is beneficial because it attacks all foreign invaders that are not part of the cell’s self.


An immune response can usually be described generally as "The reaction of the host's immune system to antigen in an invading (infecting) pathogenic organism, or to foreign protein, as in transplanted organs or tissues. The response is humoral and local; antibod[ies] produced by B cells combine... with antigen in an antigen-antibody complex to inactivate or neutralize antigen. This defensive mechanism often effectively controls infection."[4] An immune response is divided into 2 parts; innate and adaptive.

The innate immune response is "the response by the host that comprises the cells and mechanisms that defend the host from infection by other organisms or is activated by endogenous molecules, in a nonspecific manner."[5] The innate immune response is quick and is the body's initial response to unwanted invaders. It consists of the body's non-specific external and internal defense mechanisms. An example of the body's external defense mechanisms are mucus and skin. Skin consists of epithelial and endothelial cells which acts a sort of barrier against infection, invading antigens would have to pass through the initial skin barrier in order to actually get inside the host. Mucous acts similarly to skin, in that it is a barrier of sorts. Mucus traps invading pathogens and sometimes degrades them, preventing them from going any further into the body. Non-specific internal defense mechanisms are put in place in case the invading pathogens gets past the external defenses and actually makes it inside the body. Things such as phagocytes, and Natural Killer (NK) cells attack the pathogen and destroys it before further infection takes place.

The adaptive immune response is the body's second line of defense."Adaptive immunity has evolved to provide a broader and more finely tuned repertoire of recognition for both self- and nonself-antigens. Adaptive immunity involves a tightly regulated interplay between antigen-presenting cells and T and B lymphocytes, which facilitate pathogen-specific immunologic effector pathways, generation of immunologic memory, and regulation of host immune homeostasis."[6] 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 certain antigens. This is extremely important for B and T-cell activation. B and T cells are extremely dangerous cells, if they are able to attack without going through a rigorous process of activation, a faulty B or T cell can begin exterminating the host's own healthy cells. Every B and T-cell is different, making way for a diverse community of cells ready to recognize and attack a full range of invaders. This response is much slower than the body's innate response because its cells are so specific and require to be activated before it is able actually act. "In addition to specificity, another principal feature of adaptive immunity is the generation of immunologic memory. During the first encounter with an antigen (pathogen), sets of long-lived memory T and B cells are established. In subsequent encounters with the same pathogen, the memory cells are quickly activated to yield a more rapid and robust protective response".[6] This feature of the adaptive immune response is responsible for the development of vaccines as well as other modern day medicines targeted at disease prevention. Immunologic memory is the basic concept behind the modern day flu shot. The flu shot basically is giving the recipient a dormant flu virus. This activates the recipient's immune response. After the immune response, immunologic memory is activated, so if the individual ever comes into contact with the flu virus again the body will be prepared to deal with it accordingly, this time faster, and more efficiently.

Natural killer cellsEdit

NK cells attack self cells that have become infected rather than attack foreign invaders. NK cells have cytotoxic chemicals in which recognize a broad spectrum of foreign invaders which is non-specific. NK cells are bound to foreign substances and insert their cytotoxic chemical which results in the foreign cells to die. NK cells are a type of lymphocyte. In an organism, B and T lymphocytes are present. They grow in the bone marrow and in the liver and produce hematopoetic stem cells. [7]

Natural killer T cells (NKT)Edit

Natural killer T cells are a branch of T cells and a lymphocyte that is involved in the innate response. NKT cells can pinpoint nonpeptide antigens using MHC molecules from CD1 on the cell surface. NKT constantly express T-cell and NK cell antigens.  Invariant NKT cells express a unique TCRa rearrangement, Va24-Ja18 with Vb11 that is expressed that characterizes many NKT cells. When NKT cells are activated, cytokines are rapidly produced. IL-4 is associated in allergy pathogenesis.[6] Ulcerative colitis, UC, is a form of inflammatory bowel disease, it has recently been found that natural killer T cells can play a key role in the disease. According to a recent study, by manipulating natural killer T cells, it may be possible to modify the abnormal immunoresponse activity characteristic within UC.[8]


  1. ^ King RC, Stransfield WD (1998). Dictionary of genetics. New York, Oxford: Oxford University Press. ISBN 978-0-19-50944-1-1.
  2. ^ a b Hadžiselimović R, Pojskić N (2005). Uvod u humanu imunogenetiku / Introduction to Human Immunogenetics. Sarajevo: INGEB. ISBN 978-9958-9344-3-8.
  3. ^ Lawrence E, ed. (1999). Henderson's Dictionary of Biological Terms. London: Longman. ISBN 978-0-582-22708-8.
  4. ^ Porta MS, Last JM (2018). A Dictionary of Public Health (2nd ed.). Oxford University Press. p. 236. ISBN 978-0-19-184438-6.
  5. ^ Vincent J, Hall JB, eds. (2012). Encyclopedia of Intensive Care Medicine. Berlin, Heidelberg: Springer Berlin Heidelberg. doi:10.1007/978-3-642-00418-6. ISBN 978-3-642-00417-9.
  6. ^ a b c Bonilla FA, Oettgen HC (February 2010). "Adaptive immunity". The Journal of Allergy and Clinical Immunology. 125 (2 Suppl 2): S33–40. doi:10.1016/j.jaci.2009.09.017. PMID 20061006.
  7. ^ "Britannica Academic". Retrieved 2018-12-03.
  8. ^ Jie, Lai Li, Shen Jun, and Ran Zhi Hua. "Natural Killer T Cells and Ulcerative Colitis." Cellular Immunology (2018)Journal in ScienceDirect

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