02598nas a2200361 4500000000100000008004100001260001300042653001500055653001000070653002300080653001900103653002100122653001100143653001100154653002200165653002500187653002500212653002600237653000900263653001600272653002400288653001800312653003200330100001300362700001700375700001400392245017700406856004100583300001100624490000700635520158000642022001402222 1993 d c1993 Jun10aAdolescent10aAdult10aC-Reactive Protein10aConcanavalin A10aErythema Nodosum10aFemale10aHumans10aImmunosuppression10aLeprosy, lepromatous10aLeprosy, Tuberculoid10aLymphocyte Activation10aMale10aMiddle Aged10aPhytohemagglutinins10aT-Lymphocytes10aTumor Necrosis Factor-alpha1 aFoss N T1 aOliveira E B1 aSilva C L00aCorrelation between TNF production, increase of plasma C-reactive protein level and suppression of T lymphocyte response to concanavalin A during erythema nodosum leprosum. uhttp://ila.ilsl.br/pdfs/v61n2a06.pdf a218-260 v613 a

The complex symptoms observed in lepromatous leprosy patients with reactive episodes of the erythema nodosum leprosum (ENL) type are associated with different serum components actively participating in the acute inflammatory reaction. Among them are the tumor necrosis factor (TNF) and the acute-phase protein C-reactive protein (CRP). TNF and CRP were found at significantly more elevated concentrations in the serum of patients with ENL, with a positive correlation of about 95% when compared with patients with nonreactive lepromatous leprosy (L) or tuberculoid leprosy (T) or with control individuals. Furthermore, in another series of experiments CRP had a specific and significant suppressive action on concanavalin A (ConA)-induced lymphoproliferation in cultures from patients and controls, the reduction being more marked (75%) in patients with ENL. By extrapolation from its known actions, production of TNF may have a number of potential consequences for the immunobiology of ENL. Thus, TNF may cause direct injury to compromised cells, facilitating mononuclear cell activation and production of cytokines such as interleukin-1 and interleukin-6, and upregulating hepatocyte expression of CRP. Both CRP and TNF in high serum concentrations have the ability to enhance the acute inflammatory process in ENL, favoring increased macrophage activation and phagoctyosis, and contributing to the elimination of damaged cells and bacilli, as well as in the reduction of T-suppressor cells, with a consequent improvement in the immunologic response of ENL patients.

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