Molecular Mimicry- How your gut bacteria trick your immune system!


60 second summary

  • Some bacteria have proteins on their surface which mimic those on our own cells
  • They play a crucial role in preventing gut related inflammatory diseases.

The gut and immunity

It has been known for a while that the gut plays a large role in protection against disease: About 80% of the immune system resides inside the gut[1] alongside your microbial community, which also play a protective role by several mechanisms such as  regulation of T cells.[2]

T cells- cells playing a vital role in defense against pathogens .

T cells can distinguish between disease causing cells and safe cells via antigens.

Antigens-molecules found on cells providing information about whether or not the cell is dangerous or infected- in short deciding its fate- should it stay alive?

Recent evidence has shown that some bacteria serve a protective function through mimicking our own antigens.

IGRP206–214   is an antigen found in mice found on cells in the pancreas called islets of Langerhans cells. These cells play a large role in the control of blood sugar levels and development of diseases such as diabetes. One of the functions of this IGPR antigen is to encourage the activity of a subset of immune cells called CD8+ T cells.

CD8+ T cells- (also known as cytotoxic lymphocytes) kill infected cells by mechanisms such as release of toxic granules called perforins into the cell leading to its death.[3]

One of the functions of CD8+T cell is to suppress disease by targeting the destruction of cells presenting the foreign antigens rather than the pancreas’ beta cells.

A type of antigen on the microbial strain Bacteroides called Bacteroides Integrase has been shown to mimic the IGPR protein.  [4]

Quick introduction to Bacteroides

Bacteroides are a species generally beneficial as long as they’re residing inside the gut. However when they esacpe can cause bacteremia which is the presence of bacteria in the bloodstream which is dangerous. Generally these microbes play important roles ,such as in terms of digestion, by fermenting carbohydrates so that can be used as host energy souce. Germ free animals need 30% more calories to maintain body mass than normal mice.

Function of bacterial integrase

The integrase protein found on Bacteroides therefore is able to mimic the IGRP antigen and induce the T cells to kill infected cells rather that the body’s own insulin producing cells which is one of the causes of diabetes.

Another effect of the Bacteroides integrase in mimicking the IGPR antigen is reduction of colitis.

Colitis- inflammation of inner lining of colon. [7]

The mechanism behind this is as follows: Like IGPR, Bacteroides integrase recruits CD8+ cells. This reduces colitis because the stimulated CD8+ cells target inflammation inducing cells called dendritic cells .

Dendritic cells- antigen presenting cells which can lead to the stimulation of an immune response.

One way in which these cells cause inflammation is by over production of TNF alpha which is a molecule also associated with premature cell death. [5]

Overall this contributes to maintenance of a normal immune system.

[1] Institute of health sciences. (n.d.). Probiotics help as 80% of Immune System in your GI Tract. [online] Available at:

Probiotics help as 80% of Immune System in your GI Tract
[Accessed 13 Jul. 2019].

[2] BMJ journals. (2018). Imitation is the best form of… treating IBD?. Available at: [Accessed 13 Jul. 2019].

[3] British society of Immunology. (n.d.). CD8+ T Cells. Available at:élulas/cd8-t-cells [Accessed 13 Jul. 2019].

[4] MassiveSci. (n.d.). How gut bacteria manipulates your immune system – by mimicking it. Available at: [Accessed 13 Jul. 2019]./

[5] Wikipedia. (2019). Tumour necrosis factor. [online] Available at: [Accessed 13 Jul. 2019].

[6]Research gate. (2017). A Gut Microbial Mimic that Hijacks Diabetogenic Autoreactivity to Suppress Colitis. [online] Available at: [Accessed 13 Jul. 2019].

[7] MedicineNet. (n.d.). Colitis. [online] Available at: [Accessed 13 Jul. 2019].

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