Immunopathology of American cutaneous leishmaniasis

Pirmez, Claude

doi:10.1590/s0074-02761992000900016

Cited by 25 publications

(30 citation statements)

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“…The population of T lymphocytes present in the granulomatous infiltrate of the lesion of tegumentary leishmaniasis was mainly composed by CD4+ cells, and a lower proportion of CD8+ cells 6,9,22,25 . The subtypes of CD4+ T cells (Th1 and Th2 profile) have been characterized by many investigators in all forms of tegumentary leishmaniasis.…”

Section: Discussionmentioning

confidence: 96%

Cytokine profile in Montenegro skin test of patients with localized cutaneous and mucocutaneous leishmaniasis

Nogueira

Goto

Sotto

et al. 2008

Rev. Inst. Med. trop. S. Paulo

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SuMMarYAmerican tegumentary leishmaniasis presents as two major clinical forms: localized cutaneous leishmaniasis (LCL) and mucocutaneous leishmaniasis (MCL). The immune response in leishmaniasis is efficiently evaluated by the response to Leishmania antigen through the Montenegro skin test (MST). Both LCL and MCL present positive response to MST, indicating that the patients present cell-mediated immunity against the parasite -Leishmania. In spite of the presence of immunity in MCL, this is not sufficient to stop disease progression and prevent resistance to treatment. In this study we demonstrated interleukin (IL) 2, 4, 5 and interferon (IFN) gamma expression in biopsies of MST of ten patients with American tegumentary leishmaniasis. The obtained results were compared between LCL (n = 5) and MCL (n = 5) patients. The MST of MCL patients displayed a higher expression of IL-2, IL-4 and IL-5, in comparison to LCL. There was no significant difference in IFN-gamma expression between groups. The obtained results suggest the role of IL-4 and IL-5 in the maintenance of the immunopathogenic mechanism of the destructive lesions that characterize MCL.

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Section: Discussionmentioning

confidence: 96%

Cytokine profile in Montenegro skin test of patients with localized cutaneous and mucocutaneous leishmaniasis

Nogueira

Goto

Sotto

et al. 2008

Rev. Inst. Med. trop. S. Paulo

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“…Local immunologic abnormalities could be responsible and tissue aggression due to poor regulation of the host defense mechanisms could have an important role, but conclusive data are required. 10 However, neither explanation can account for the long periods of mucosal granuloma quiescence after maximal drug treatment before relapse. The possibility of reinfection is not likely since relapse always occurred at the same mucosal sites and no new skin lesions were noted.…”

Section: Discussionmentioning

confidence: 99%

Clinical observations of unresponsive mucosal leishmaniasis.

Marsden

Lessa²,

Oliveira³

et al. 1998

The American Journal of Tropical Medicine and Hygiene

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Abstract. We report the long-term clinical follow-up of two patients with unresponsive mucosal leishmaniasis due to Leishmania (Viannia) braziliensis from the Três Braços area in Bahia State, Brazil. Both were agricultural male workers with extensive upper respiratory mucosal involvement that was not cured with conventional and experimental therapy.In 1985, we reported two male patients with unresponsive mucosal leishmaniasis who appeared to respond to continuous antimony therapy. 1 At that time, we did not realize how long follow-up was necessary to pronounce clinical cure and both patients subsequently relapsed. In 1986, we reported a recurrence in one of these patients. 2 We now report their long-term follow-up to the end of 1996. Given that a parasitologic cure is difficult to prove and may never occur in some forms of leishmaniasis, 3 response to treatment and relapse were established based on clinical criteria of granuloma activity followed by confirmatory biopsy. All parasite isolations identified by monoclonal antibodies and isoenzyme taxonomy have been Leishmania (Viannia) braziliensis. The last clinical evaluation 1996 showed active mucosal granulomata despite all available treatment. This is the justification for the title of this paper. One of us (PDM) had followed these patients for 18 years. Despite recurrences after treatment, recent granulomata seem less aggressive. Both patients do not have any associated disease or condition such as tuberculosis, schistosomiasis, or blastomycosis, that can explain their peculiar evolution, which we have seen complicating recovery from L. (V.) braziliensis infection in humans. These patients lead normal lives and have growing families. They have spent long periods as hospital inpatients and are not anxious to re-enter the hospital. A brief update of their case histories is given with a tabulated summary of treatment regimens. CASE REPORTSPatient MB (LTB12), a 42-year old man, developed mucosal granulomata at the age of 20. He had no history or sign of a cutaneous lesion. The nose, both palates, and the larynx were affected. Leishmania (Viannia) braziliensis was isolated from a nasal mucosal lesion and characterized by isoenzymes and monoclonal antibodies in 1984 and has been reisolated seven times during the last 20 years. He always responded well to antimony therapy only to relapse. After our last report, he relapsed two years later and subsequent treatment is detailed in Table 1. In our previous report, he appeared to have responded to 85 days of therapy with sodium stibogluconate (Pentostam; Wellcome, London, United Kingdom) (20 mg/kg/day) in the hospital to the tolerance limit. 1 In 1996, he had active granulomata around the nasal septal perfuration confirmed by histology. He also had gran-*Deceased. uloma on the right inferior turbinate and a immunofluorescent antibody titer of 1:80. In our laboratory, a titer Ͼ 1:20 is regarded as significant. Mucosal surfaces affected over time include the nasal septum, inferior turbinates, hard and soft palates, orophary...

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“…High percentages of activated cells expressing CD62L high , LFA-1a and LFA-1b are found in peripheral blood in comparison to the lymph nodes of CL patients in the early stages of the disease, suggesting that these cells are available for recruitment to lesion sites [15]. The percentage of skin cells presenting CLA is very low, comprising less than one-third of the cells from CL [14,29], which is surprising considering the high percentage of memory T cells in the inflammatory infiltrate [4]. Differences in the expression of migration molecules in CD4 + and CD8 + T cells indicate that there are specific requirements for the homing of these cells to a leishmaniasis lesion [13,15,26].…”

Section: Introductionmentioning

confidence: 97%

“…The skin lesions are characterized by a chronic granulomatous inflammatory infiltrate consisting mainly of lymphocytes, plasmocytes and histiocytes [3]. Memory T lymphocytes predominate in lesions [4], but the proportions of T CD4 + and T CD8…”

Section: Introductionmentioning

confidence: 99%

“…Several reports have suggested that a huge influx of T cells takes place in lesions [4,7,8], as not only is a higher frequency observed of local lymphocytes responding to L. braziliensis in comparison with blood [9], but also an increased proportion of T CD4 + and T CD8 + cells is reported in older lesions [5,6]. Although the effector T cell response mounted in response to the parasite can lead to a cure, it also seems to be responsible for tissue damage [10,11].…”

Section: Introductionmentioning

confidence: 99%

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The skin homing receptor cutaneous leucocyte-associated antigen (CLA) is up-regulated byLeishmaniaantigens in T lymphocytes during active cutaneous leishmaniasis

Mendes-Aguiar¹,

Gomes-Silva²,

Nunes

et al. 2009

Clinical and Experimental Immunology

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SummaryThe cutaneous leucocyte-associated antigen receptor (CLA) can direct Leishmania-specific T lymphocytes towards inflamed skin lesions. Homing receptors [CLA, lymphocyte-associated antigen 1 (LFA-1) or CD62L] were analysed in lymphocytes from blood and cutaneous leishmaniasis (CL) lesions. CL patients with active lesions (A-CL) presented lower levels of T lymphocytes expressing the CLA + phenotype (T CD4 + = 10·4% Ϯ 7·5% and T CD8 + = 5·8% Ϯ 3·4%) than did healthy subjects (HS) (T CD4 + = 19·3% Ϯ 13·1% and T CD8 + = 21·6% Ϯ 8·8%), notably in T CD8 + (P < 0·001). In clinically cured patients these percentages returned to levels observed in HS. Leishmanial antigens up-regulated CLA in T cells (CLA + in T CD4 + = 33·3% Ϯ 14·1%; CLA + in T CD8 + = 22·4% Ϯ 9·4%) from A-CL but not from HS. An enrichment of CLA + cells was observed in lesions (CLA + in T CD4 + = 45·9% Ϯ 22·5%; CLA + in T CD8 + = 46·4% Ϯ 16·1%) in comparison with blood (CLA + in T CD4 + = 10·4% Ϯ 7·5%; CLA + in T CD8 + = 5·8% Ϯ 3·4%). Conversely, LFA-1 was highly expressed in CD8+ T cells and augmented in CD4+ T from peripheral blood of A-CL patients. In contrast, CD62L was not affected. These results suggest that Leishmania antigens can modulate molecules responsible for migration to skin lesions, potentially influencing the cell composition of inflammatory infiltrate of leishmaniasis or even the severity of the disease.

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Immunopathology of American cutaneous leishmaniasis

Cited by 25 publications

References 0 publications

Cytokine profile in Montenegro skin test of patients with localized cutaneous and mucocutaneous leishmaniasis

Cytokine profile in Montenegro skin test of patients with localized cutaneous and mucocutaneous leishmaniasis

Clinical observations of unresponsive mucosal leishmaniasis.

The skin homing receptor cutaneous leucocyte-associated antigen (CLA) is up-regulated byLeishmaniaantigens in T lymphocytes during active cutaneous leishmaniasis

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