CD4+ and/or γδ+ T cells in the liver spontaneously produce IL-4 in vitro during the early phase of Leishmania major infection in susceptible BALB/c mice

Yamashita, T; Miyata, Hiroaki; Miyaji, Chikako; Watanabe, Hirotaka; Abo, Toru; Kobayakawa, Takatoshi; Kaneko, Akira; Sendo, Fujiro

doi:10.1016/s0001-706x(99)00014-5

Cited by 8 publications

(4 citation statements)

References 22 publications

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“…Additional host-strain differences have been found in the manner in which parasites disseminate from the site of inoculation to the draining lymph nodes and visceral organs; dissemination occurs rapidly in BALB/c mice, whereas early parasite containment in the footpad and draining lymph nodes is observed in resistant mice 33 . As a result of this dissemination, CD4 + T cells that produce IL-4 spontaneously in vitro can be found in the liver and spleen of BALB/c mice two weeks after infection, whereas these cells are not found in the viscera of C57BL/6 mice 34 . The same distinctive patterns of early parasite trafficking have been observed recently in a comparison of BALB/c SCID and C57BL/6 SCID mice, which indicates that the differences are not secondary to an adaptive immune response (T. Kamala and P. Matzinger, personal communication).…”

Section: Il-12: Redirecting the Early T H 2 Responsementioning

confidence: 99%

The immunology of susceptibility and resistance to Leishmania major in mice

2002

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Established models of T-helper-2-cell dominance in BALB/c mice infected with Leishmania major -- involving the early production of interleukin-4 by a small subset of Leishmania-specific CD4+ T cells -- have been refined by accumulating evidence that this response is not sufficient and, under some circumstances, not required to promote susceptibility. In addition, more recent studies in L. major-resistant mice have revealed complexities in the mechanisms responsible for acquired immunity, which necessitate the redesign of vaccines against Leishmania and other pathogens that require sustained cell-mediated immune responses.

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Section: Il-12: Redirecting the Early T H 2 Responsementioning

confidence: 99%

The immunology of susceptibility and resistance to Leishmania major in mice

2002

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“…The fact that the same distinctive patterns of parasite dissemination were observed in BALB/c severe combined immunodeficiency disease ( scid ) and C57Bl/6 scid mice indicates that they are not the result of differences in the early adaptive response (T. Kamala & P. Matzinger, unpublished observations). One result of this dissemination is that CD4 + T cells can be found in the livers and spleens of 2‐week‐infected BALB/c mice that spontaneously produce IL‐4 in vitro , whereas these cells are not found in the viscera of C57BL/6 mice (50). The influence of the site of antigen delivery on Th‐lineage commitment has been clearly demonstrated in the L. major model; parasites delivered intravenously or intranasally can elicit Th2 responses and produce non‐healing visceral infections in normally resistant mice (51, 52).…”

Section: Balb/c Mice Have Intrinsic Defects In Th1 Differentiationmentioning

confidence: 99%

Section: Balb/c Mice Have Intrinsic Defects In Th1 Differentiationmentioning

confidence: 99%

Re‐examination of the immunosuppressive mechanisms mediating non‐cure of Leishmania infection in mice

Sacks

Anderson

2004

Immunological Reviews

122

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The interleukin (IL)-4 driven, polarized T-helper 2 cell (Th2) response that controls non-healing infection with Leishmania major in BALB/c mice has long been embraced as the underlying principle with which to consider the pathogenesis of non-healing and systemic forms of leishmaniasis in humans. The inability, however, to reveal a Th2 polarity associated with non-curing clinical disease has suggested that alternative cells and cytokines are involved in susceptibility. In this review, various mouse models of non-curing infection with L. major and other Leishmania species are re-examined in the context of the suppression mediated by IL-10 and regulatory T (Treg) cells. These activities are revealed in L. major-infected BALB/c IL-4 knockout (KO) and IL-4Ralpha KO mice and especially in non-cure resistant mice that do not default to a Th2 pathway as a result of inherent defects in Th1 differentiation. In contrast to the extreme BALB/c susceptibility arising from an aberrant Th2 response, non-cure in resistant mice arises from an imbalance in Treg cells that are activated in the context of an ongoing Th1 response and whose primary function may be to suppress the immunopathology associated with persistent antiparasite responses in infected tissues.

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“…Consistently, it was shown in many clinical and experimental settings that γδ T cells have the potential to produce type 2 cytokines. To name just a few, such cells were found in mice and human beings during pregnancy, 22 , 23 in the airways of human patients with asthma 24 and in mouse models of asthma, 14 , 25 , 26 among human clones specific for cypress pollen lipid allergens, 27 in the liver of BALB/c mice infected with Leishmania major , 28 and among early tumor infiltrating lymphocytes in a mouse model of melanoma 29 . Why all these different conditions induce T H2 ‐like γδ T cells is not clear.…”

Section: Th2 Immunity and γδ T Cellsmentioning

confidence: 99%

Balanced approach of γδ T cells to type 2 immunity

et al. 2010

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Substantial evidence has been accumulated to indicate that cd T cells take part in type 2 immune responses. It is not yet clear, however, in what capacity. Apparently, cd T cells themselves can not only take the function of follicular T helper (T H ) cells in certain responses, but also can support responses that are dependent on classical help provided by ab T cells. Furthermore, the cd T cells engage as regulators of T H2 immunity. Here, we consider two mouse models that depend on type 2 immunity, nonspecific airway hyperresponsiveness to methacholine after allergen inhalation challenge and the primary IgE response induced by alum-aided immunization, and examine the function of cd T cells. In either case, cd T cells regulate type 2 immunity through balanced enhancing and inhibitory influences. However, after airway allergen exposure, suppressive cd T cells become dominant. The underlying mechanisms are discussed.

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CD4+ and/or γδ+ T cells in the liver spontaneously produce IL-4 in vitro during the early phase of Leishmania major infection in susceptible BALB/c mice

Cited by 8 publications

References 22 publications

The immunology of susceptibility and resistance to Leishmania major in mice

The immunology of susceptibility and resistance to Leishmania major in mice

Re‐examination of the immunosuppressive mechanisms mediating non‐cure of Leishmania infection in mice

Balanced approach of γδ T cells to type 2 immunity

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