Augmentation of Intestinal and Peripheral Natural Killer Cell Activity During the Graft-Versus-Host Reaction in Mice

Borland, Annette; Mowat, Allan Mc.I.; Parrott, Delphine M. V.

doi:10.1097/00007890-198311000-00009

Cited by 38 publications

(14 citation statements)

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“…This might be explained by any increased presence of activated NK cells secreting IFN-␥. NK cells have been described in systemic tissues as early as day 3 (58 -60) and among intestinal IEL during GVHR (61). NK cell functions among cells from PP, MLN, and LP have not been reported for the acute GVHR model.…”

Section: Discussionmentioning

confidence: 99%

Early Intestinal Th1 Inflammation and Mucosal T Cell Recruitment During Acute Graft-Versus-Host Reaction

Snider

Liang

2001

The Journal of Immunology

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Little is understood about the earliest cytokine responses and the role(s) of donor CD4 T cells in the intestine during the induced graft-vs-host reaction (GVHR). We investigated the activation and mucosal homing phenotype of the donor CD4 cells and the kinetics of cytokine responses within the intestine and associated lymphoid tissues during early GVHR. Significant frequencies of donor CD4 cells accumulated within recipient Peyer’s patches (PP), mesenteric lymph nodes (MLN), lamina propria (LP), and spleen (SP), during the first 9 days of GVHR. Many donor CD4 cells in SP, MLN, and LP expressed CD44 and also expressed de novo the mucosal homing integrin α4β7 (LPAM-1). A large IFN-γ response occurred by day 3 in cells from PP and MLN, but much later (day 9) in SP and LP cells. IL-10 production by SP and MLN cells was elevated initially but declined substantially by day 9. IL-4 production by SP, MLN, and PP cells was low on day 3 and showed gradual decline in LP by day 9. IL-5 production by LP cells gradually increased in direct contrast to IL-5 production by MLN cells. The MLN CD4 cells showed the most dynamic changes, with high numbers of activated/effector donor CD4 cells and altered cytokine production consistent with a developing Th1 response. The IFN-γ responses in PP and MLN preceded that of the SP, suggesting an intestinal origin for some Th1 effector cells in GVHR. Donor CD4 T cells apparently acquire the ability to home to the LP during early GVHR.

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Section: Discussionmentioning

confidence: 99%

Early Intestinal Th1 Inflammation and Mucosal T Cell Recruitment During Acute Graft-Versus-Host Reaction

Snider

Liang

2001

The Journal of Immunology

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“…Under these conditions engrafted lymphocytes become sensitized to host alloantigens and generate a variety of specific and nonspecific cell-mediated cytotoxic responses. Although cytotoxic T cells have been deemed to be the principal effectors of tissue injury (12), there is a growing body of evidence that macrophages (13) and natural killer cells (14)(15)(16) may also be involved. Since lymphoid cells are particularly well endowed with both class I and class I1 histocompatibility antigens on their surfaces, it is not surprising that with GVHD there is a major assault on organs of the immune system such as the spleen, the lymph nodes, and mucosal-associated lymphoid tissues.…”

Section: Discussionmentioning

confidence: 99%

Thymic Involution with Loss of Hassall's Corpuscles Mimicking Thymic Dysplasia in a Child with Transfusion-Associated Graft-Versus-Host Disease

Gartner

1991

Pediatric Pathology

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A 7-year-old leukemic girl developed pancytopenia following chemotherapy and was given several transfusions of nonirradiated blood. Within 2 weeks she developed a maculopapular rash, fever, abnormal liver function, diarrhea, and wasting. She became septic and died 6 weeks later. Transfusion-associated graft-versus-host disease (GVHD) was suspected clinically. At autopsy, changes diagnostic of GVHD were present in the skin and liver. The remarkable feature of the case was the histopathology of the thymus, which was morphologically "dysplastic," i.e., minute, lymphoid depleted, devoid of a corticomedullary demarcation, and completely lacking in Hassall's corpuscles. These changes were virtually identical to those seen in the thymus of children with severe combined immunodeficiency disease (SCID). There was no evidence of preexisting immune deficiency. There is compelling experimental evidence that GVHD can produce changes in the thymus that are identical to those of "thymic dysplasia." These observations have led to the hypothesis that immunodeficiency associated with GVHD may stem, in part, from injury to thymic epithelium resulting in defective T cell maturation. As a corollary of this hypothesis, it has been suggested that the pathogenesis of some forms of SCID may involve GVHD-associated injury to the thymus by a maternal allograft acquired in utero. This report further documents thymic pathology in human GVHD and discusses these changes in the light of these ideas.

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“…The role of soluble factors was further suggested by the identification of natural killer cells in the 1EL of this model [53] which could be activated by interferon or interlcukin-2.…”

Section: Pathogenesis Of Intestinal Injury With Acute Gvhdmentioning

confidence: 96%

Destruction of the Intestinal Mucosa after Bone Marrow Transplantation and Graft-versus-Host Disease

Beschorner¹

1984

Pathol Immunopathol Res

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Augmentation of Intestinal and Peripheral Natural Killer Cell Activity During the Graft-Versus-Host Reaction in Mice

Cited by 38 publications

References 0 publications

Early Intestinal Th1 Inflammation and Mucosal T Cell Recruitment During Acute Graft-Versus-Host Reaction

Early Intestinal Th1 Inflammation and Mucosal T Cell Recruitment During Acute Graft-Versus-Host Reaction

Thymic Involution with Loss of Hassall's Corpuscles Mimicking Thymic Dysplasia in a Child with Transfusion-Associated Graft-Versus-Host Disease

Destruction of the Intestinal Mucosa after Bone Marrow Transplantation and Graft-versus-Host Disease

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