Genetic background influences immune responses and disease outcome of cutaneous L. mexicana infection in mice

Rosas, Lucia E.; Keiser, Tracy L.; Barbi, Joseph; Satoskar, Anjali A.; Septer, Alecia N.; Kaczmarek, Jennifer; Lezama-Dávila, Claudio M.; Satoskar, Abhay R.

doi:10.1093/intimm/dxh313

Cited by 62 publications

(60 citation statements)

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“…Another possibility to explain the controversial role of IFN-γ involves the cell source of this cytokine. Since in CBA/J mice the increase in IFN-γ-producing-CD8 + T cells is involved with protection against the disease (Rosas et al 2005) and MHCII (-/-) mice is refractory to L. amazonensis infection (Soong et al 1997), it kill intracellular amastigotes (Green et al 1990, Reiner & Locksley 1995. The observation that MHC II (-/-), RAG2 (-/-), SCID mice (Soong et al 1997) and CD4 + -depleted BALB/c mice (Silva et al 1994) are refractory to L. amazonensis infection raises the possibility that CD4 + T cells contribute to the pathogenesis of L. amazonensis.…”

Section: Discussionmentioning

confidence: 99%

“…This is of relevance since the pathogenesis caused by L. amazonensis in humans follows a pattern different from that described for L. major and has been associated not only with localized cutaneous lesions but also with diffuse cutaneous leishmaniasis and more rarely, fatal visceral leishmaniasis (Convit et al 1993, Almeida et al 1996. Notably, in Colmenares et al 2003, Rosas et al 2005.…”

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confidence: 96%

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Interferon-gamma is required for the late but not early control of Leishmania amazonensis infection in C57Bl/6 mice

Pinheiro

Rossi-Bergmann

2007

Mem. Inst. Oswaldo Cruz

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The critical role of interferon-gamma (IFN-γ) in the resistance of C57Bl/6 mice to Leishmania major is widely established but its role in the relative resistance of these animals to L. amazonensis infection is still not clear. In this work we use C57Bl/6 mice congenitally deficient in the IFN-γ gene (IFN-γ KO) Leishmaniasis is a complex of diseases caused by the obligate intracellular protozoan parasites of the genus Leishmania. The various clinical forms of human leishmaniasis have been partially reproduced in different strains of mice. For example, C57Bl/6 mice infected with L. major develop cutaneous lesions that spontaneously heal, whereas BALB/c mice harbor non-healing cutaneous lesions. Such experimental models have earlier allowed definition of some of the immunological factors involved in resistance and susceptibility to L. major infection (Reiner & Locksley 1995). During L. major infection of mice, a polarized differentiation of Th1/Th2 CD4 + T cells occurs in resistant and susceptible mice and the Th1 cytokine interferon-γ (IFN-γ) plays an essential role in controlling parasite growth and disease progression (Scott 1991, Liew et al. 1997. Evidence for the critical role for IFN-γ in the control of L. major infection comes from the demonstration that IFN-γ knockout (KO) mice fail to cure infection (Wang et al. 1994).In contrast to L. major, the immunological mechanisms determining susceptibility and resistance to L. amazonensis have been less studied. This is of relevance since the pathogenesis caused by L. amazonensis in humans follows a pattern different from that described for L. major and has been associated not only with localized cutaneous lesions but also with diffuse cutaneous leishmaniasis and more rarely, fatal visceral leishmaniasis (Convit et al. 1993, Almeida et al. 1996. Notably, in IFN-γ production by CD8 + T cells has been associated with immunoregulatory responses induced by leishmanial antigens that elicit significant protection against L. amazonensis (Champsi & McMahon-Pratt 1988, Soong et al. 1997) and an overproduction of IFN-γ seems necessary for development of a resistant phenotype (Afonso & Scott 1993). The protective role of IFN-γ in L. amazonensis infection is further questioned in a more recent report showing that IFN-γ promotes the replication of L. amazonensis amastigotes in macrophages, as opposed to its inhibitory effect on L. major infected macrophages (Qi et al. 2004). In vivo, adoptive transfer of naïve splenocytes devoid of CD4 + CD25 + Treg cells into RAG1-/-mice before infection markedly exacerbated disease progression, and this effect was associated with a marked production of IFN-γ by the effector T cells (Ji et al. 2005). Since the role of IFN-γ during L. amazonensis infection is not a resolved issue, in the present work we proposed to evaluate the course of L. amazonensis infection in IFN-γ KO mice. MATERIALS AND METHODSMice -C57Bl/6-background IFN-γ KO mice were a kind gift of Dr Leda Quércia Vieira (Gnotobiology Laboratory, Federal University of Minas Gerais,...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 96%

Interferon-gamma is required for the late but not early control of Leishmania amazonensis infection in C57Bl/6 mice

Pinheiro

Rossi-Bergmann

2007

Mem. Inst. Oswaldo Cruz

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“…In both human and experimental models of CL, control of infection is mediated by T-lymphocytes and is critically dependent upon the early induction of an IL-12-driven Th-1 type immune response and the production of IFN-c by CD4 T cells (Rosas et al 2005;Tripathi et al 2007).…”

Section: Gamma-interferon (Ifn-c)mentioning

confidence: 99%

Comparative immune study on cutaneous leishmaniasis patients with single and multiple sores

2013

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Ninety-five Iraqi patients with cutaneous leishmaniasis (CL) caused by Leishmania tropica at AL-Karama Hospital in Baghdad were included in this study. Sixty patients were with single sore and the remaining with multiple sores. The study also included 10 atopic patients and 30 healthy individuals as a control group. Cellular and humoral immune response at different stages of the disease activity (early and late) were evaluated by estimation of serum IFNc, IL-4 and total IgE antibodies using ELISA kits while, the detection of specific anti leishmanial IgE antibodies was done manually. Specific IgE antibodies were only detected in early CL (\2 months) patients 68 (71.57 %) while, were not detected in late CL, atopic and healthy controls 30 (100 %). The results also showed a positive relationship between this antibody and the number of sores. Th-2 predominates during the early stage of the disease then shifts to Th-1 that proceed in the late stage, but both cytokines increased in CL patients in comparison to control group. The immune response of CL infection is possibly regulated by both Th-1 and Th-2. Multiple sores patients showed an increase of anti leishmanial IgE (0.120 ± 0.014), total IgE (120.7 ± 39.58 IU/ml), IFN-c (87.4 ± 30.52 pg/ml) and IL-4 (63.70 ± 20.32 pg/ml) levels than single sore patients with mean value of 0.108 ± 0.14, 92.3 ± 35.23 IU/ml, 47.2 ± 27.80 pg/ml and 51.04 ± 15.0 pg/ml respectively. It can be presented also as ratio of INF-c/IL-4 = 1.37 which is greater than those for single sore 0.9. These results indicated that the immune response of multiple sores patient's is higher than that with single sores.

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“…16,25 Herein filaggrin-deficient mice were generated on a BALB/c background, a strain predisposed to type 2/type 17-associated inflammation. [17][18][19][40][41][42] Increased NF-kB activity in nonlesional skin of Flg ft/ft mice indicates basal subclinical cutaneous inflammation. Indeed, although relatively modest, the increased IL-4, IL-17, and IFNg protein levels in nonlesional skin demonstrated a generalized subclinical inflammatory milieu in the skin.…”

Section: Discussionmentioning

confidence: 99%

March to the beat of adaptive immunity

Singh

2015

Sci. Transl. Med.

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Genetic background influences immune responses and disease outcome of cutaneous L. mexicana infection in mice

Cited by 62 publications

References 31 publications

Interferon-gamma is required for the late but not early control of Leishmania amazonensis infection in C57Bl/6 mice

Interferon-gamma is required for the late but not early control of Leishmania amazonensis infection in C57Bl/6 mice

Comparative immune study on cutaneous leishmaniasis patients with single and multiple sores

March to the beat of adaptive immunity

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