LEPROMATOUS AND TUBERCULOID LEPROSY - CLINICAL PRESENTATION AND CYTOKINE RESPONSES

Citation
Mt. Ochoa et al., LEPROMATOUS AND TUBERCULOID LEPROSY - CLINICAL PRESENTATION AND CYTOKINE RESPONSES, International journal of dermatology, 35(11), 1996, pp. 786-790
Citations number
22
Categorie Soggetti
Dermatology & Venereal Diseases
ISSN journal
00119059
Volume
35
Issue
11
Year of publication
1996
Pages
786 - 790
Database
ISI
SICI code
0011-9059(1996)35:11<786:LATL-C>2.0.ZU;2-Y
Abstract
Objective. This study analyzes the major clinical characteristics of p atients with active leprosy in relation to the in vitro immune respons e to the T-lymphocyte activator anti-CD3. Methods. Thirty-eight patien ts with an established diagnosis of leprosy were classified according to the Ridley and Jopling table. Peripheral blood mononuclear cells fr om both lepromatous leprosy (LL) and tuberculoid leprosy (TL) patients and healthy controls were used to evaluate lymphocyte proliferation; immunoenzymatic assays were used to evaluate cytokine production (IL-1 , IL-2, IL-4, IL-6, IL-10, IFN-gamma). Results. Peripheral blood monon uclear cells from both LL and TL patients displayed blastogenic respon ses to anti-CD3. The cytokines IL-1 beta, IL-6, IL-10, and IFN-gamma w ere detected in culture supernatants. Endogenous production of IL-18 w as significantly higher in cell cultures from patients with the leprom atous form of the disease compared to those with tuberculoid leprosy. Production of IL-6 in response to anti-CD3 was observed in a significa ntly higher proportion of LL than TL patients (P = 0.0025). Gamma-inte rferon production did not differ between TL and LL, but a direct corre lation was observed between time of multidrug treatment and IFN produc tion in vitro (P = 0.016). Interleukin-10 was detected in culture supe rnatants of lymphocytes activated by anti-CDS from both patient groups , but not from healthy controls. Conclusions. The findings of this stu dy suggest that patients with the two distinct forms of leprosy are ca pable of responding to a polyclonal T-lymphocyte stimulus such as anti -CD3 and provide evidence suggestive of alterations in the immune resp onses mediated by cytokines that may contribute to the spectrum of dis ease and response to treatment.