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Humoral immune response to Helicobacter pylori:
Generic humoral immune response:
The humoral immune system is a component of the adaptive immune system. It refers to the portion of immunity that B cells are responsible for. B cells, will recognize the appropriate antigen from their surface receptors, but will not interact to neutralize or destroy the antigen. After recognizing an antigen, B cells migrate to the secondary lymphoid tissue and proliferate to form daughter lymphocytes, which are identical to the original B cell. These B cells then develop into short-lasting plasma cells. The plasma cells serve to produce antibodies and release them into the blood. However, some activated B-cells will not develop into plasma cells but will instead become memory cells. Unlike plasma cells, memory cells are long-lasting and will continue to produce small amounts of antibody long after the infection has been cleared. These memory cells allow for immunological memory, where the immune system has a much easier time staging a defense against a pathogen it has already had contact with.
The antibodies produced and secreted by the plasma cells are Y shaped and contain binding sites for specific antigen found on the surfaces of viruses and bacteria. Once the antibody binds to antigen, it flags the complex for destruction by phagocytes. Five types of antibodies exist. IgG is the most predominant antibody and it implements the compliment cascade. The next most predominant antibody is IgA which is found in mucous secretion. IgE is unique as it contains 5 binding sites. IgM and IgE are the least predominant and play roles in suppressing lymphocyte activity and allergic responses, respectively.
Figure 1: General humoral immune response
Humoral immune response specific to H. pylori:
Studies have shown that there is an increased number of plasma cells in the gastric mucosa where H. pylori resides revealing that the body presents an active humoral immune response against the bacteria. The anti- H. pylori antibodies produced are primarily of the IgG type. However, in is also common for the IgA antibody to be circulating in infected people. Specifically, levels of IgG1, IgG2 and IgG4 are elevated in infected people while IgG3 antibodies that are associated with acute infection are not detected. Furthermore, serological testing showed that IgG antibodies binded best to H. Pylori antigen with IgA have the second best sensitivity to the antigen.
While antibodies such as IgG and IgA are produced to combat H. pylori, their effectiveness is debated. Some studies provide evidence that shows these antibodies decrease both the bacterial growth and toxicity of H. pylori. However, other studies provide evidence that shows that antibodies against H. pylori react with gastric mucosa. The amount of these antibodies against self or auto-antibodies have been shown to by proportional to the degree of gastritis in infected individuals. Furthermore, studies suggest that the Lewis antigens present in the bacteria’s LPS could cause the stimulation of antibodies that react against the gastric mucosa.
With respect to the complement aspect of the humoral immune response, Helicobacter pylori is sensitive to complement and can even activate the classical complement pathway without the presence of antibodies. H. pylori activate the classical complement pathway because its LPS generate large amounts of C3b. However, this C3b may also lead to destruction of gastric mucosa cells, which leads to gastric mucosa.
A common theme relating to the body’s immune response to H. pylori is that the immune response also kills gastric mucosa self cells. Killing these cells cause peptic ulcers and pain to the infected individual.
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.
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