This webpage was produced as an assignment for an undergraduate course at Davidson College.
Cellular immune response to Helicobacter pylori:
Generic cellular immune response:
Cellular immunity along with humoral immunity comprise the adaptive immune response. Unlike humoral immunity that involves B cells and antibodies, cellular immunity responds to antigen by the activation of macrophages, cytotoxic T cells, CD4 T cells, natural killer (NK) cells in addition to the release of cytokines. The cytotoxic T cells or CD8 cells directly destroy infected cells. Cytotoxic T cells recognize cells infected with viruses or intracellular bacteria that express markers on their cell surface and will kill these infected cells before the virus inside has time to replicate. CD4 TH1 cells respond to bacteria infected cells by activating macrophages to phagocytose the infected cell. CD4 TH1 cells also secrete cytokines and chemokines which flag the area of infection and attract macrophages to this site. CD4 TH2 cells also recognize antigen or infected cells and activate B cells and the humoral immune response. Finally, this cellular immune response plays a large role in combating virus infection, intracellular bacteria and is responsible for transplant rejection.
Figure 1: The generic cellular immune response.
Cellular immune response specific to H. pylori:
The cellular immune system does respond to H. pylori as evident by an increase in the number of CD4 cells, macrophages and dendritic cells in the gastric mucosa of individuals infected with the bacteria. Like the humoral and innate immune response, the cellular immune response serves to damage the epithelia lining of the stomach causing ulcers. H. pylori infection corresponds with a TH1 cell type response where there is an overproduction of interferon (IFN)-γ. IFN- γ is a cytokine which attracts macrophages and NK cells. When IFN-γ is overproduced, it attracts too many lethal macrophages and NK cells which produce enzyme and free radicals which don’t just kill the infected cells but also kill the cells around them by inducing apoptosis. Therefore, this overproduction of IFN-γ leads to the killing a gastric mucosal cells and ulcers. However, studies have shown that T regulatory cells (CD4+CD25+) play a role in limiting gastritis caused by the cellular immune response. T regulatory cells reduce the activation of CD4+ cells that produce IFN-γ. Yet, by lowering the production of IFN-γ, more H. pylori is allowed to survive.
In addition to the overproduction of IFN- γ, the production of pro-inflammatory cytokines damages the stomach’s epithelial lining. H. pylori LPS induces the release of pro-inflammatory cytokines IL-1β, IL-6, IL-8 and TNF-α. These cytokines lead to inflammation which in turn leads to injury of the gastric mucosal cells. Similar to the humoral and innate immune response, the body’s cellular immune response to H. pylori bacteria cause damage to the gastric musocal cells which leads to stomach ulcer and gastritis.
Helicobacter Pylori Infection, Immune Response and Vaccination. A. Lembo, L. Caradonna, T. Magrone, M. L. Mastronardi, D. Caccavo, E. Jirillo, L. Amati.
NIH Consensus Statement: Helicobacter pylori in Peptic Ulcer Disease. Vol 12, Number 1. February 7-9, 1994.
Immunobiology: The Immune System in Health and Disease 6th ed. Charles A. Janeway Jr. et al. 2005
Contact information: firstname.lastname@example.org