One of my lost abstracts re: dysfunctional Th1 response triggered by borrelia

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http://www.jci.org/cgi/content/full/97/4/1028

Therefore, although it may be advantageous to mount Th1 responses to

control infections by intracellular pathogens, this strategy is not

particularly effective against B. burgdorferi, an organism that may

be predominantly extracellular. Protection against B. burgdorferi

infection requires the generation of borreliacidal antibodies

directed against certain spirochete antigens, including outer

surface protein (Osp) A and B (34, 35), and is therefore influenced

by B cell help provided by Th2 type CD4+ T cells. Thus, the

induction of a predominant Th1 response may be a mechanism utilized

by the spirochete to reduce, in part, appropriate T cell responses

that can facilitate efficient antibody production and therefore

avoid host defenses. Moreover, the maintenance of a Th1 inflammatory

response, which leads to destruction of certain tissues where the

spirochete resides might be an important source of nutrients.

The finding that the treatment with anti- IL-12 decreases the Th1

responses in vivo and consequently the degree of acute disease,

indicates that the development of this type of T cell response is

responsible for some of the arthritis that results from spirochetal

infection. Th1 responses are produced during human Lyme disease (9,

10), suggesting a correlation between the development of Th1

responses against B. burgdorferi and the severity of human Lyme

disease. Our results would indicate that immune responses that can

be blocked by anti-IL-12 contribute to the pathogenesis of acute

murine Lyme arthritis. It is likely, therefore, that B. burgdorferi

specific Th1 responses influence the evolution of murine and human

Lyme borreliosis.