Open AccessAntigens of Lyme disease of spirochaete Borrelia burgdorferi inhibits antigen or mitogen‐induced lymphocyte proliferation
Author(s) -
Chiao J.W.,
Pavia Charles,
Riley Michael,
AltmannLasekan Wendy,
Abolhassani Moshen,
Liegner K.,
Mittelman Abraham
Publication year - 1994
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.1994.tb00437.x
Subject(s) - pokeweed mitogen , borrelia burgdorferi , spirochaete , biology , antigen , immune system , concanavalin a , microbiology and biotechnology , lymphocyte , immunology , t lymphocyte , lyme disease , cellular immunity , antibody , in vitro , bacteria , biochemistry , genetics
Modulation of cellular immune responses by the spirochaete Borrelia burgdorferi , the bacteria that causes Lyme disease, was demonstrated. When cultured in the presence of sonicated Borrelia preparation (Bb), the mitogen‐ or antigen‐stimulated proliferative responses of normal lymphocytes were consistently lowered. Bb caused the greatest reduction in Concanavalin A (ConA) or antigen‐stimulated proliferation, where almost 100% reduction in proliferation could be achieved. Bb also reduced phytohemagglutinin‐M (PHA) or pokeweed mitogen (PWM)‐stimulated peripheral blood lymphocyte (PBL) proliferation, with the PWM proliferation being the least affected. This regulatory activity was not due to toxicity and was determined to be caused by Bb protein antigens. The degree of the proliferation reduction was directly proportional to both Bb quantity and length of exposure to lymphocytes. IL‐2 production was significantly reduced from Bb‐exposed lymphocytes. The entry of lymphocytes into the proliferating phases of the cell cycle was also shown to be blocked. These results have demonstrated an immune suppressive mechanism of B. burgdorferi . The magnitude of host immune responses may be dependent on the degree of suppression which is related to the spirochaete quantity and their length of presence in the host.