Phenotypic and functional profiling of malaria-induced CD8 and CD4 T cells during blood-stage infection with Plasmodium yoelii

Chandele, Anmol; Mukerjee, Paushali; Das, Gobardhan; Ahmed, Rafi; Chauhan, Virander S.

doi:10.1111/j.1365-2567.2010.03363.x

Cited by 45 publications

(56 citation statements)

References 54 publications

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“…We then examined the effects of these cytokines on CD4 T-cell development during blood-stage malaria. The lack of defined CD4 T-cell epitopes has hindered efforts to characterize CD4 T-cell function during malaria, and we therefore used cell proliferation as a surrogate for identifying CD4 T cells that respond to PbA infection (26). In these experiments, T-cell proliferation was detected by expression of the nuclear protein Ki67.…”

Section: Il-12 and Ifn-γ Interfere With The Development Of T-cell-medmentioning

confidence: 99%

APlasmodium-encoded cytokine suppresses T-cell immunity during malaria

Sun¹,

Holowka²,

Song³

et al. 2012

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

116

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The inability to acquire protective immunity against Plasmodia is the chief obstacle to malaria control, and inadequate T-cell responses may facilitate persistent blood-stage infection. Malaria is characterized by a highly inflammatory cytokine milieu, and the lack of effective protection against infection suggests that memory T cells are not adequately formed or maintained. Using a genetically targeted strain of Plasmodium berghei, we observed that the Plasmodium ortholog of macrophage migration inhibitory factor enhanced inflammatory cytokine production and also induced antigen-experienced CD4 T cells to develop into short-lived effector cells rather than memory precursor cells. The short-lived effector CD4 T cells were more susceptible to Bcl-2–associated apoptosis, resulting in decreased CD4 T-cell recall responses against challenge infections. These findings indicate that Plasmodia actively interfere with the development of immunological memory and may account for the evolutionary conservation of parasite macrophage migration inhibitory factor orthologs.

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Section: Il-12 and Ifn-γ Interfere With The Development Of T-cell-medmentioning

confidence: 99%

APlasmodium-encoded cytokine suppresses T-cell immunity during malaria

Sun¹,

Holowka²,

Song³

et al. 2012

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

116

View full text Add to dashboard Cite

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“…Viral persistence is associated with loss of effector functions by CD4 and CD8 T cells, generally referred to as "exhaustion" (1,2). Exhausted T-cell responses have been reported in tumor settings as well as in parasitic and bacterial infection (3)(4)(5)(6)(7). The clone 13 strain of lymphocytic choriomeningitis virus (LCMV cl13) is an excellent tool for studying chronic infection because the exhausted T-cell phenotype is molecularly similar to that observed in serious human chronic infections and tumor immunity (1).…”

mentioning

confidence: 99%

PTPN22 contributes to exhaustion of T lymphocytes during chronic viral infection

Maine

Teijaro

Marquardt

et al. 2016

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

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The protein encoded by the autoimmune-associated protein tyrosine phosphatase nonreceptor type 22 gene, PTPN22, has wide-ranging effects in immune cells including suppression of T-cell receptor signaling and promoting efficient production of type I interferons (IFN-I) by myeloid cells. Here we show that mice deficient in PTPN22 resist chronic viral infection with lymphocytic choriomeningitis virus clone 13 (LCMV cl13). The numbers and function of viral-specific CD4 T lymphocytes is greatly enhanced, whereas expression of the IFNβ-induced IL-2 repressor, cAMP-responsive element modulator (CREM) is reduced. Reduction of CREM expression in wild-type CD4 T lymphocytes prevents the loss of IL-2 production by CD4 T lymphocytes during infection with LCMV cl13. These findings implicate the IFNβ/CREM/IL-2 axis in regulating T-lymphocyte function during chronic viral infection.

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“…Plasmodium-specific CD4+ T cells not only are important as a source of IFN-γ but are also essential for activation of both CD8+ T cells and B cells. It is widely accepted that B cells and CD4+ T cells are mainly activated during the blood stage infection and CD8+ T cells are activated during the pre-erythrocytic or liver stage of the Plasmodium life cycle [21,22].…”

Section: Introductionmentioning

confidence: 99%

Immune responses during gestational malaria: a review of the current knowledge and future trend of research

Maestre

Carmona‐Fonseca

2014

J Infect Dev Ctries

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Women pregnant with their first child are susceptible to severe P. falciparum disease from placental malaria because they lack immunity to placenta-specific cytoadherence proteins. In subsequent pregnancies, as immunity against placental parasites is acquired, there is a reduced risk of adverse effects of malaria on the mother and fetus and asymptomatic parasitaemia is common. In the case of vivax malaria, with increasing reports of severe cases in Asia and South America, the effects of infection by this species during pregnancy remain to be elucidated. This review summarized the main aspects involved in the acquisition of specific antimalarial immune responses during pregnancy with emphasis in research carried out in America and Asia, in order to offer a framework of interpretation for studies on pregnant women with malaria which are recently being produced in these regions. The authors conclude that (1) Effective humoral responses during gestational malaria are mainly directed against variant surface antigens codified by genes of the var2Csa family of P. falciparum; (2) Acquisition of immunity against these variant antigens depends on the degree and intensity of transmission, and the chance increases with age and successive pregnancies; (3) Antibody development is guided by specific cellular immune responses in cases of placental and maternal infection, and (4) The study of the significance of acquisition of specific immunity against both P. falciparum and P. vivax in America, should be performed.

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Phenotypic and functional profiling of malaria-induced CD8 and CD4 T cells during blood-stage infection with Plasmodium yoelii

Cited by 45 publications

References 54 publications

APlasmodium-encoded cytokine suppresses T-cell immunity during malaria

APlasmodium-encoded cytokine suppresses T-cell immunity during malaria

PTPN22 contributes to exhaustion of T lymphocytes during chronic viral infection

Immune responses during gestational malaria: a review of the current knowledge and future trend of research

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