Immune response to Mycoplasma pneumoniae

Mycoplasma pneumoniae has protein as well as glycolipid antigens that provoke antibody responses in those who are affected by the infection. One of the most common aims pursued by many antibodies generated by the host in response to the Mycoplasma pneumoniae infection is P1 protein. After an initial infection the immune system starts quickly generating antibodies. The peak comes in 3 to 6 weeks time. Then a decline is observed that can last for months and even years. Since the incubation period is rather longish, the response to antibodies can be observed when the symptoms reveal themselves.

The rise in Mycoplasma pneumoniae-specific IgM in the majority of cases can be regarded as a sign of severe infection, for it emerges within the first week of the incubation period and about a couple of weeks before IgG antibody does. At the same time, it is more applicable in pediatric populations when there is a minimal chance of repeated exposures. In case with adults who have been endured infections repeatedly it can happen that they will not have any reaction to mycoplasma antigens with a quick IgM response. Thus, reinfection causes an IgG response.

There is also IgA antibody, which is often underestimated and not paid attention to in the process of diagnosis. However, it can be more efficient in identifying recent infections in groups of all ages. This type of antibodies is generated in the early stage of the disease. It is also by a rapid elevation to peak levels, and decline that happens before that of IgM or IgG.

Apart from Mycoplasma pneumoniae-specific antibodies, there is a whole row of cross-reactive antibodies that can appear during Mycoplasma pneumoniae infection. There is an extensive sequence homology of the Mycoplasma pneumoniae adhesin proteins and glycolipids of the cell membrane with mammalian tissues. They are able to cause autoimmune disorders that affect multiple organ systems in a way of creating antibodies against such substances as myosin, keratin, fibrinogen, brain, liver, kidney, smooth muscle, and lung tissues.

There are also a number of acid homologies with human CD4 and class II major histocompatibility complex lymphocyte proteins. They function as producers of autoreactive antibodies and causers of cellular damage and immune system suppressors.

Infection caused by Mycoplasma pneumoniae also includes specific T-cell-mediated immunity. Thus, lymphocytes from persons who have already had the infection earlier, will be subjected to blast transformation in case of Mycoplasma pneumoniae. Leukocytes from those who suffer from Mycoplasma pneumoniae infections will also have chemotaxis symptoms when the organism is present. In this case, a person will have a response in the form of IFN- presence in the blood.

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