Effector Functions of Antibody and CD8+Cells in Resolution of Rotavirus Infection and Protection against Reinfection in Mice

McNeal, Monica; Barone, K.Siobhan; Rae, Mary N.; Ward, Richard L.

doi:10.1006/viro.1995.0048

Cited by 109 publications

(130 citation statements)

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“…The first notion is supported by delayed clearance of rotavirus in infected MT compared with J H D mice, both on the H-2 b background (31). B cell deficiency also manifests itself differently during distinct infections.…”

Section: Discussionmentioning

confidence: 95%

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Mechanisms of Central Nervous System Viral Persistence: the Critical Role of Antibody and B Cells

Ramakrishna

Stohlman

Atkinson

et al. 2002

The Journal of Immunology

111

168

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Contributions of humoral and cellular immunity in controlling neurotropic mouse hepatitis virus persistence within the CNS were determined in B cell-deficient JHD and syngeneic H-2d B cell+ Ab-deficient mice. Virus clearance followed similar kinetics in all mice, confirming initial control of virus replication by cellular immunity. Nevertheless, virus reemerged within the CNS of all Ab-deficient mice. In contrast to diminished T cell responses in H-2b B cell-deficient μMT mice, the absence of B cells or Ab in the H-2d mice did not compromise expansion, recruitment into the CNS, or function of virus-specific CD4+ and CD8+ T cells. The lack of B cells and lymphoid architecture thus appears to manifest itself on T cell responses in a genetically biased manner. Increasing viral load did not enhance frequencies or effector function of virus-specific T cells within the CNS, indicating down-regulation of T cell responses. Although an Ab-independent antiviral function of B cells was not evident during acute infection, the presence of B cells altered CNS cellular tropism during viral recrudescence. Reemerging virus localized almost exclusively to oligodendroglia in B cell+ Ab-deficient mice, whereas it also replicated in astrocytes in B cell-deficient mice. Altered tropism coincided with distinct regulation of CNS virus-specific CD4+ T cells. These data conclusively demonstrate that the Ab component of humoral immunity is critical in preventing virus reactivation within CNS glial cells. B cells themselves may also play a subtle role in modulating pathogenesis by influencing tropism.

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Section: Discussionmentioning

confidence: 95%

“…T cell activation following microbial infections or immunization of these mice is comparable to wt mice (31)(32)(33). Similar to infected MT mice (25), JHMV was initially cleared from the CNS but subsequently reactivated in both B cell/Ab-deficient and Ab-only-deficient mice.…”

mentioning

confidence: 83%

Mechanisms of Central Nervous System Viral Persistence: the Critical Role of Antibody and B Cells

Ramakrishna

Stohlman

Atkinson

et al. 2002

The Journal of Immunology

111

168

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“…As RV-specific antibody responses are observed in T cell receptor-deficient mice (27) and CD8 + T cells accelerate RV clearance (23,42), we repeated our αPDCA-1 antibody treatment regimen followed by oral RV infection in CD8-deficient animals to assess the role of pDCs in the induction of RV-specific fecal IgA during acute infection independent of the CD8 + T cell response. As observed in the serum, RV-specific fecal IgA production was significantly diminished following infection in αPDCA-1-treated CD8 knockout mice ( Figure 6A).…”

Section: Pdcs Are Necessary and Sufficient For Human B Cell Activatiomentioning

confidence: 99%

Plasmacytoid dendritic cells promote rotavirus-induced human and murine B cell responses

Deal

Lahl²,

Narváez³

et al. 2013

J. Clin. Invest.

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B cell-dependent immunity to rotavirus, an important intestinal pathogen, plays a significant role in viral clearance and protects against reinfection. Human in vitro and murine in vivo models of rotavirus infection were used to delineate the role of primary plasmacytoid DCs (pDCs) in initiating B cell responses. Human pDCs were necessary and sufficient for B cell activation induced by rotavirus. Type I IFN recognition by B cells was essential for rotavirus-mediated B cell activation in vitro and murine pDCs and IFN-α/β-mediated B cell activation after in vivo intestinal rotavirus infection. Furthermore, rotavirus-specific serum and mucosal antibody responses were defective in mice lacking functional pDCs at the time of infection. These data demonstrate that optimal B cell activation and virus-specific antibody secretion following mucosal infection were a direct result of pDC-derived type I IFN. Importantly, viral shedding significantly increased in pDC-deficient mice, suggesting that pDC-dependent antibody production influences viral clearance. Thus, mucosal pDCs critically influence the course of rotavirus infection through rotavirus recognition and subsequent IFN production and display powerful adjuvant properties to initiate and enhance humoral immunity.

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“…However, adoptive transfer of CD8 ϩ T cells into SCID mice results in clearance of RV with a short delay compared with normal mice (15), suggesting that clearance can occur in the absence of B cells or Abs and that control of RV infection can occur at the cellular level. Further evidence for a B cell/Ab-independent clearance mechanism is provided by studies that demonstrated that RV infection in B cell-deficient JHD and Mt mice was efficiently cleared (16). Taken together, these studies in knockout (KO) mice have implicated both B and T lymphocyte subsets in rotaviral clearance, but within the context of an intact immune system the lymphocyte subsets critical for clearance have not been identified.…”

mentioning

confidence: 99%

Early Response to Rotavirus Infection Involves Massive B Cell Activation

Blutt¹,

Warfield²,

Lewis

et al. 2002

The Journal of Immunology

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Rotavirus is an acute enteric pathogen which induces severe diarrhea in infants and children. To determine the immune response to rotavirus in vivo, we used a mouse model of rotavirus infection. We observed dramatic increases in the sizes of both Peyer’s patches and mesenteric lymph nodes, but not spleen, between 1 and 6 days after infection with a homologous strain of murine rotavirus, EC wild type. Histological analysis showed large increases in the numbers of lymphocytes in these same tissues in rotavirus-infected mice. Flow cytometric analysis confirmed the increase in numbers of lymphocytes and revealed a large increase in the percentage of activated B, but not T, lymphocytes in both Peyer’s patches and mesenteric lymph nodes of rotavirus-infected mice compared with control mice. Fragment cultures from these tissues established at 3–4 days postinfection contain rotavirus-specific IgM but not IgA Ab. A similar degree of lymphoid hyperplasia and percentage of activated B cells were observed in rotavirus-infected TCR knockout mice. Taken together, our findings show that rotavirus infection, in the context of a normal immune response, induces a large increase in the percentages of activated B cells in the absence of any detectable increase in the percentage of activated T cells, implicating a T cell-independent B cell response as the primary mechanism for initial rotavirus clearance.

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Effector Functions of Antibody and CD8+Cells in Resolution of Rotavirus Infection and Protection against Reinfection in Mice

Cited by 109 publications

References 0 publications

Mechanisms of Central Nervous System Viral Persistence: the Critical Role of Antibody and B Cells

Mechanisms of Central Nervous System Viral Persistence: the Critical Role of Antibody and B Cells

Plasmacytoid dendritic cells promote rotavirus-induced human and murine B cell responses

Early Response to Rotavirus Infection Involves Massive B Cell Activation

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