The immunobiology of XXXX .

@entity1 @entity1203 @entity3761 @entity308 @entity66 @entity102 @entity4430 @entity1199 @entity1201
@entity1201 , a @entity102 of @entity1 , is caused by the obligate intracellular bacterium @entity4430 . Infection with @entity4430 affects the peripheral nerves and the dermis, causing an accumulation of macrophages and other immune cells at the infected sites. Host resistance to the bacterium determines the extent of local inflammatory reactions and its resulting damage to the affected tissues. In @entity66 little if any cellular immunity develops. Bacterial multiplication is uncontrolled and @entity4430 disseminate throughout most of the dermis. In @entity66 , marked cellular immunity is observed and bacterial growth and dissemination are controlled. The @entity308 of cellular immunity in @entity1203 @entity1 is not fully understood. Since @entity4430 cannot be grown in vitro, and a suitable animal model has not yet been developed, the study of host immunity to the pathogen is limited primarily to investigations of the cutaneous lesions of @entity1 and to in vitro responses of the peripheral blood leukocytes to @entity4430 . While the blood monocytes of @entity1201 @entity1 appear to be activated normally by lymphokines, T cell proliferation and production of lymphokines in response to @entity4430 are impaired in @entity1203 @entity1 . Attempts to restore responsiveness in cells from these @entity1 have been unsuccessful in our hands. The addition of exogenous @entity1199 to leukocyte cultures does not appear to restore responsiveness to @entity4430 in cells from nonresponsive @entity1 . Rather, some enhancement, often not antigen specific, is observed in cells from @entity1 with a preexisting response. Similarly, depletion of monocytes does not restore responsiveness to @entity4430 in nonresponder @entity1 , but a nonspecific enhancement of proliferation is observed in monocyte-free cultures from @entity1 that do respond to @entity4430 . Thus, the defect in @entity1203 @entity1 does not result from a simple lack of @entity1199 production or suppression by monocytes and/or their products. Possibly, there is a low level or lack of @entity4430 -responsive T cells in the circulation of these @entity1 . Attempts to overcome the defect in immunity of @entity1 with @entity1203 by immunoprophylaxis and immunotherapy are being investigated. This approach has become of major importance since the development of widespread drug resistance to @entity3761 as well as to the other chemotherapeutic agents used to control @entity1201 .
