Resistance to Malarial Infection Is Achieved by the Cooperation of NK1.1+ and NK1.1− Subsets of Intermediate TCR Cells Which Are Constituents of Innate Immunity

Mannoor, M. Kaiissar; Weerasinghe, Anura; Halder, Ramesh C.; Reza, Sufi; Morshed, M.; Ariyasinghe, Anoja; Watanabe, Hirotaka; Sekikawa, Hiroho; Abo, Toru

doi:10.1006/cimm.2001.1833

Cited by 43 publications

(40 citation statements)

References 52 publications

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“…We have previously reported that both NKT cells and NK1.1 Ϫ CD3 int cells were stimulated by malarial infection, although the expansion of NK1.1 Ϫ CD3 int cells was much more dominant (25). This result was confirmed by two-color staining for CD3 and NK1.1 in the liver of B6 mice (Fig.…”

Section: Details Of the Phenotypic Characterization Of Lymphocytes Thsupporting

confidence: 70%

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Essential Role of Extrathymic T Cells in Protection Against Malaria

Mannoor

Halder

Morshed

et al. 2002

The Journal of Immunology

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Athymic nude mice carry neither conventional T cells nor NKT cells of thymic origin. However, NK1.1−TCRint cells are present in the liver and other immune organs of athymic mice, because these lymphocyte subsets are truly of extrathymic origin. In this study, we examined whether extrathymic T cells had the capability to protect mice from malarial infection. Although B6-nu/nu mice were more sensitive to malaria than control B6 mice, these athymic mice were able to survive malaria when a reduced number of parasitized erythrocytes (5 × 103 per mouse) were injected. At the fulminant stage, lymphocytosis occurred in the liver and the major expanding lymphocytes were NK1.1−TCRint cells (IL-2Rβ+TCRαβ+). Unconventional CD8+ NKT cells (Vα14−) also appeared. Similar to the case of B6 mice, autoantibodies (IgM type) against denatured DNA appeared during malarial infection. Immune lymphocytes isolated from the liver of athymic mice which had recovered from malaria were capable of protecting irradiated euthymic and athymic mice from malaria when cell transfer experiments were conducted. In conjunction with the previous results in euthymic mice, the present results in athymic mice suggest that the major lymphocyte subsets associated with protection against malaria might be extrathymic T cells.

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Section: Details Of the Phenotypic Characterization Of Lymphocytes Thsupporting

confidence: 70%

“…When we observed immunoparameters in mice infected with Plasmodium, there was no evidence of the activation of conventional T cells (i.e., TCR high cells) (24,25). Rather, these mice showed thymic atrophy during malarial infection, suggesting the arrest of conventional T cell differentiation.…”

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confidence: 82%

Essential Role of Extrathymic T Cells in Protection Against Malaria

Mannoor

Halder

Morshed

et al. 2002

The Journal of Immunology

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“…Studies in mice using mouse Plasmodium strains have shown that mouse immune cells such as natural killer (NK) cells, T cells, dendritic cells, and B cells all contribute to antiparasitic immunity (7)(8)(9)(10). Notably, depletion of NK cells in a mouse model of Plasmodium chabaudi infection results in more severe disease associated with higher parasitemia and mortality (11).…”

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confidence: 99%

Human natural killer cells control Plasmodium falciparum infection by eliminating infected red blood cells

Chen

Amaladoss

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Immunodeficient mouse-human chimeras provide a powerful approach to study host-specific pathogens, such as Plasmodium falciparum that causes human malaria. Supplementation of immunodeficient mice with human RBCs supports infection by human Plasmodium parasites, but these mice lack the human immune system. By combining human RBC supplementation and humanized mice that are optimized for human immune cell reconstitution, we have developed RBC-supplemented, immune cell-optimized humanized (RICH) mice that support multiple cycles of P. falciparum infection. Depletion of human natural killer (NK) cells, but not macrophages, in RICH mice results in a significant increase in parasitemia. Further studies in vitro show that NK cells preferentially interact with infected RBCs (iRBCs), resulting in the activation of NK cells and the elimination of iRBCs in a contact-dependent manner. We show that the adhesion molecule lymphocyte-associated antigen 1 is required for NK cell interaction with and elimination of iRBCs. Development of RICH mice and validation of P. falciparum infection should facilitate the dissection of human immune responses to malaria parasite infection and the evaluation of therapeutics and vaccines. malaria infection | humanized mouse model | LFA-1 | NK killing

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“…12 The present results remind us of previous data indicating that a major factor involved in malarial protection might be innate immunity mediated by extrathymic T cells in the liver (TCRint cells). [1][2][3][13][14][15] Nucleated erythrocytes infected with malarial parasites still express MHC antigens on their cell surface. 2 Certain autoantigens or malarial antigens inserted into MHC might be recognized by TCRint on extrathymic T cells, and such interaction would induce innate immunity.…”

Section: Discussionmentioning

confidence: 99%

“…4 Briefly, the liver was removed, pressed through a 200-gauge stainless steel mesh, and suspended in Eagle's MEM (Nissui Pharmaceutical, Tokyo, Japan) supplemented with 5 mmol/L HEPES and 2% heat-inactivated newborn calf serum. After being washed once with medium, cells were fractionated by centrifugation in 15 …”

Section: Cell Preparationmentioning

confidence: 99%

Protection against malaria by anti‐erythropoietin antibody due to suppression of erythropoiesis in the liver and at other sites

et al. 2005

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SummaryWe have previously reported that erythropoiesis commences in the liver and spleen after malarial infection, and that newly generated erythrocytes in the liver are essential for infection of malarial parasites as well as continuation of infection. At this time, erythropoietin (EPO) is elevated in the serum. In the present study, we administered EPO or anti-EPO antibody into C57BL/6 (B6) mice to modulate the serum level of EPO. When mice were infected with a non-lethal strain (17NXL) of Plasmodium yoelii (blood-stage infection of 10 4 parasitized erythrocytes per mouse), parasitemia continued for 1 month, showing a peak at day 17. Daily injection of EPO (200 IU/day per mouse) from day five to day 14 prolonged parasitemia, whereas injection of anti-EPO antibody (1.5 mg/day per mouse) every second day from day five to day 28 decreased it. Erythropoiesis was confirmed in the liver, spleen and bone marrow by the appearance of nucleated erythrocytes (TER119+). When anti-EPO antibody was injected by the same protocol into mice infected with a lethal strain (17XL) of P. yoelii , all mice showed decreased parasitemia and recovered from the infection. These results suggest that the use of anti-EPO antibody after malarial infection may be of therapeutic value in severe cases of malaria.

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Resistance to Malarial Infection Is Achieved by the Cooperation of NK1.1+ and NK1.1− Subsets of Intermediate TCR Cells Which Are Constituents of Innate Immunity

Cited by 43 publications

References 52 publications

Essential Role of Extrathymic T Cells in Protection Against Malaria

Essential Role of Extrathymic T Cells in Protection Against Malaria

Human natural killer cells control Plasmodium falciparum infection by eliminating infected red blood cells

Protection against malaria by anti‐erythropoietin antibody due to suppression of erythropoiesis in the liver and at other sites

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