Cytokine Production by Vγ<sup>+</sup>-T-Cell Subsets Is an Important Factor Determining CD4<sup>+</sup>-Th-Cell Phenotype and Susceptibility of BALB/c Mice to Coxsackievirus B3-Induced Myocarditis

Huber, Sally A.; Graveline, Danielle; Born, Willi K.; O’Brien, Rebecca L.

doi:10.1128/jvi.75.13.5860-5869.2001

Cited by 77 publications

(79 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…injection of 0.2 ml of PBS containing 10 4 PFU of CVB3 H3 or H310A1 variants as described previously (9). Virus titers in tissues or in in vitro cell populations were determined by the plaque-forming assay as described earlier.…”

Section: Virus Virus Infection and Virus Titrationmentioning

confidence: 99%

“…Isolation of cell populations has been described previously (9). Briefly, spleens were pressed through fine mesh screens, centrifuged on Histopaque-1077 (Sigma-Aldrich, St. Louis, MO), to remove RBC, and incubated on nylon wool for 30 min at 37°C.…”

Section: Isolation Of Splenic Lymphocytesmentioning

confidence: 99%

“…TNF-␣ is necessary for CVB3 pathogenicity (6 -8). A second difference between H3 and H310A1 virus infections is that only the former virus activates V␥4 ϩ T cells, which promote myocarditis susceptibility (9). ␥␦ ϩ cells comprise up to 50% of the T cell infiltrate in the hearts of H3-infected animals (8,10).…”

mentioning

confidence: 99%

“…As with ␣␤ TCR ϩ cells, ␥␦ ϩ T cells can be distinguished by their variable (V) gene usage. V␥1 ϩ T cells induce myocarditis resistance while V␥4 ϩ T cells induce susceptibility (9,11). In the present studies, we show that H3 virus infections up-regulate expression of CD1d (a nonpolymorphic MHC I-like molecule often associated with innate immunity and control of infectious agents (12)(13)(14)(15)(16)(17)(18) both in vitro on infected myocytes and in vivo in the heart.…”

mentioning

confidence: 99%

See 3 more Smart Citations

Role of CD1d in Coxsackievirus B3-Induced Myocarditis

Huber

Sartini

Exley

2003

The Journal of Immunology

View full text Add to dashboard Cite

The myocarditic (H3) variant of Coxsackievirus B3 (CVB3) causes severe myocarditis in BALB/c mice and BALB/c mice lacking the invariant Jα281 gene, but minimal disease in BALB/c CD1d−/− animals. This indicates that CD1d expression is important in this disease but does not involve the invariant NKT cell often associated with CD1d-restricted immunity. The H3 variant of the virus increases CD1d expression in vitro in neonatal cardiac myocytes whereas a nonmyocarditic (H310A1) variant does not. Vγ4+ T cells show increased activation in both H3-infected BALB/c and Jα281−/− mice compared with CD1d−/− animals. The activated BALB/c Vγ4+ T cells from H3-infected mice kill H3-infected BALB/c myocytes and cytotoxicity is blocked with anti-CD1d but not with anti-MHC class I (Kd/Dd) or class II (IA/IE) mAbs. In contrast, H3 virus-infected CD1d−/− myocytes are not killed. These studies demonstrate that CD1d expression is essential for pathogenicity of CVB3-induced myocarditis, that CD1d expression is increased early after infection in vivo in CD1d+ mice infected with the myocarditic but not with the nonmyocarditic CVB3 variant, and that Vγ4+ T cells, which are known to promote myocarditis susceptibility, appear to recognize CD1d expressed by CVB3-infected myocytes.

show abstract

Section: Virus Virus Infection and Virus Titrationmentioning

confidence: 99%

Section: Isolation Of Splenic Lymphocytesmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Role of CD1d in Coxsackievirus B3-Induced Myocarditis

Huber

Sartini

Exley

2003

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…In the early stage of infection ␥␦ T cells appear to be proinflammatory; their absence results in increased pathogen burden (6,14), and they secrete IFN-␥ (3,8,17,18) and up-regulate its production by other lymphocytes and NK cells (19,20). They can also direct adaptive (␣␤ T cell) responses (21)(22)(23). During the later stages of the immune response to microbial infection, ␥␦ T cells kill bacteria-elicited, activated macrophages, coincident with or after bacterial clearance (24), indicative of the involvement of ␥␦ T cells in preventing chronic inflammation.…”

mentioning

confidence: 99%

Delineation of the Function of a Major γδ T Cell Subset during Infection

Andrew

Newton

Dalton

et al. 2005

The Journal of Immunology

View full text Add to dashboard Cite

γδ T cells play important but poorly defined roles in pathogen-induced immune responses and in preventing chronic inflammation and pathology. A major obstacle to defining their function is establishing the degree of functional redundancy and heterogeneity among γδ T cells. Using mice deficient in Vγ1+ T cells which are a major component of the γδ T cell response to microbial infection, a specific immunoregulatory role for Vγ1+ T cells in macrophage and γδ T cell homeostasis during infection has been established. By contrast, Vγ1+ T cells play no significant role in pathogen containment or eradication and cannot protect mice from immune-mediated pathology. Pathogen-elicited Vγ1+ T cells also display different functional characteristics at different stages of the host response to infection that involves unique and different populations of Vγ1+ T cells. These findings, therefore, identify distinct and nonoverlapping roles for γδ T cell subsets in infection and establish the complexity and adaptability of a single population of γδ T cells in the host response to infection that is not predetermined, but is, instead, shaped by environmental factors.

show abstract

Evidence for the opposing roles of different γδ T cell subsets in macrophage homeostasis

et al. 2006

View full text Add to dashboard Cite

To ensure invading pathogens are eliminated with minimal damage to host tissues it is essential that macrophage activation be tightly regulated. Previously we demonstrated that a subset of gammadelta T cells (Vgamma1(+)) contributes to resolving pathogen-induced immune responses by killing activated macrophages. However, the exaggerated macrophage response seen in infected Vgamma1(+) T cell-deficient mice suggests that gammadelta T cells play a broader role in macrophage homeostasis and other subsets might promote macrophage activation. Using a macrophage:gammadelta T cell co-culture system we have shown that gammadelta T cells increase the activity of macrophages activated in vivo by Listeria monocytogenes infection. In a dose-dependent manner, gammadelta T cells up-regulated production of cytokines (TNF-alpha, IL-6, IL-10) and chemokines (MIP-1alpha, MIP-1beta) by Listeria-elicited macrophages. The ability to increase macrophage cytokine production was prominent among Vgamma4(+) gammadelta T cells. Reciprocally, Vgamma4(+) gammadelta T cells were activated by Listeria-elicited macrophages, resulting in production of the anti-inflammatory cytokine, IL-10. gammadelta T cell adoptive transfer experiments showed that Vgamma4(+) T cells protected TCRdelta(-/-) mice against Listeria-induced liver injury and necrosis. These findings identify distinct and non-overlapping roles for gammadelta T cell subsets in regulating macrophage function during pathogen-induced immune responses

show abstract

Cytokine Production by Vγ⁺-T-Cell Subsets Is an Important Factor Determining CD4⁺-Th-Cell Phenotype and Susceptibility of BALB/c Mice to Coxsackievirus B3-Induced Myocarditis

Cited by 77 publications

References 44 publications

Role of CD1d in Coxsackievirus B3-Induced Myocarditis

Role of CD1d in Coxsackievirus B3-Induced Myocarditis

Delineation of the Function of a Major γδ T Cell Subset during Infection

Evidence for the opposing roles of different γδ T cell subsets in macrophage homeostasis

Contact Info

Product

Resources

About

Cytokine Production by Vγ+-T-Cell Subsets Is an Important Factor Determining CD4+-Th-Cell Phenotype and Susceptibility of BALB/c Mice to Coxsackievirus B3-Induced Myocarditis

Cited by 77 publications

References 44 publications

Role of CD1d in Coxsackievirus B3-Induced Myocarditis

Role of CD1d in Coxsackievirus B3-Induced Myocarditis

Delineation of the Function of a Major γδ T Cell Subset during Infection

Evidence for the opposing roles of different γδ T cell subsets in macrophage homeostasis

Contact Info

Product

Resources

About

Cytokine Production by Vγ⁺-T-Cell Subsets Is an Important Factor Determining CD4⁺-Th-Cell Phenotype and Susceptibility of BALB/c Mice to Coxsackievirus B3-Induced Myocarditis