Immune Response Basics: Resistance

Immune Response Basics: Resistance

Published on Monday, October 31, 2022 by Elyse Krawtz

Immune health begins with barriers, but resistance reigns when a real threat breaches a barrier. 

Resistance encompasses all the immune responses aimed at reducing or eliminating threats. 

Resistance responses can be broadly organized into two major categories: innate and adaptive immune responses. 

Innate immune responses occur within hours and last for days, but with limited specificity. In other words, these are the first responders, so they must be ready for just about any type of credible threat. Innate immune responses activate after a barrier is breached when patrolling sensor cells detect evidence of something questionable in the area. A piece of a microbe or a high concentration of chemicals that are not supposed to be outside cells can bind to receptors on sensor cells, causing them to destroy the threat or to call for backup.

When the innate immune cells sound the alarm, they do so by inducing inflammation. Inflammation is the accumulation of fluid, plasma proteins, and immune cells initiated by injury, infection, or local immune response. 

We know inflammation when we see its five hallmarks:

  • Redness 
  • Swelling
  • Heat
  • Pain
  • Loss of function

Inflammation isn’t pleasant, but it does three essential tasks for the immune system. It brings the right cells to the battle, sets up local barriers (blood clots) so that the threat cannot escape, and begins the healing process for any damaged tissue. If the innate immune response is not enough, innate immune cells themselves will call for even more backup: adaptive immune response. 

The adaptive immune system takes days to train to fight a new threat but responds with impeccable specificity once trained. It is also poised for memory so that adaptive immune cells can act swiftly the next time the threat returns. B Cells and T Cells are the major adaptive immune cells, and both work closely together to train and strategize.

Like attacks from land, air, or sea, require different military responses, intracellular viruses or bacteria, extracellular bacteria, and parasites each require different immune resistance strategies. Therefore, adaptive immune responses are not only specific but specialized. 

Subsets of Helper T Cells facilitate different types of adaptive immune responses suited to defeat each type of microbial threat. And the training process for B cells means generating highly specific receptors called antibodies which they can release to bind different targets, thwarting their plans and marking them for destruction. 

Does immune resistance matter for someone with GI disorders like GERD or IBS? 

Absolutely! Infections, inflammation, and/or immune tolerance dysfunction could each play a role in different GERD-like or IBS symptoms. For example, acute infectious gastroenteritis is such a well-known and common IBS trigger that the resulting disease has its own title: post-infectious IBS. 

Post-infectious IBS has been associated with all types of microbial infections: viruses, bacteria, and parasitic. Mounting an effective resistance to these microbes is essential in preventing prolonged inflammation and infection. 

How can you support immune resistance? Begin by taking simple steps in these articles to support your immune barriers, gut microbiota, and overall nutrition, since all immune strategies --avoidance, resistance, and tolerance--depend on these.  


  1. Murphy K, Weaver C. (2017). Janeway’s Immunobiology. 9th ed. Garland Science/Taylor & Francis. 
  2. Punchard, N. A., Whelan, C. J., & Adcock, I. (2004). The Journal of Inflammation. Journal of inflammation (London, England), 1(1), 1. 
  3. Berumen, A., Lennon, R., Breen-Lyles, M., Griffith, J., Patel, R., Boxrud, D., Decuir, M., Farrugia, G., Smith, K., & Grover, M. (2021). Characteristics and Risk Factors of Post-Infection Irritable Bowel Syndrome After Campylobacter Enteritis. Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association, 19(9), 1855–1863.e1. 

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