CNS angiitis in graft vs host disease

Ma, M.; Barnes, Gregory; Pulliam, J.; D, Jezek; Baumann, Ralf; Berger, Joseph R.

doi:10.1212/01.wnl.0000038948.09158.a7

Cited by 72 publications

(55 citation statements)

References 8 publications

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“…[8][9][10][11][12][13] The histological pattern of inflammation was consistent with our findings concerning perivascular localization of lymphomononuclear infiltrates and glial activation. Involvement of the vessel wall was present in all of our patients, whereas transmural granulomas and occurrence of giant cells, as described earlier, 10,11 could not be detected. Meningeal vessel infiltration was also observed in one patient, but meninges were not exclusively affected as reported previously.…”

Section: Resultssupporting

confidence: 88%

“…9 In analogy with former findings, immunohistological subtyping identified the cerebral infiltrates in our patients to be monocytes and cytotoxic T cells in the majority. As in the genetic studies of Ma et al, 11 we could show that perivascular cerebral infiltrates in the brain of Patient 2 were of donor origin using the in-situ hybridization technique. This observation is consistent with the diagnosis of cerebral GVHD, as donor lymphocytes have an essential pathophysiological role in GVHD.…”

Section: Resultssupporting

confidence: 61%

“…Owing to the short follow-up period, symptoms were mild and confined to the peripheral nervous system. 3 Severe angiitis-like syndromes were reported casuistically to occur in patients with chronic GVHD, but diagnosis was based either on angiography 7 or on histological analysis, [8][9][10][11][12][13] with a heterogenous spectrum of immunohistological methods used.…”

Section: Introductionmentioning

confidence: 99%

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Cerebral angiitis in four patients with chronic GVHD

Sostak

Eigenbrod

et al. 2009

Bone Marrow Transplant

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There is growing evidence that GVHD affects the central nervous system (CNS). In this study, we describe the longterm follow-up of four allogeneic BM recipients who developed cerebral angiitis-like disease probably due to GVHD. The patients developed focal neurological signs, cognitive deficits and/or coma in association with GVHD, 2-18 years after transplantation, following reduction of immunosuppressive therapy. Magnetic resonance imaging was variable, showing generalized brain atrophy, ischemic lesions or leukoencephalopathy. Diagnosis of cerebral angiitis was confirmed by histopathological analysis of bioptic brain tissue and response to immunosuppressive therapy. By means of immunohistochemistry and immunofluorescence, perivascular lymphomononuclear cerebral infiltrates were shown to express the adhesion receptor, CD11a, and the chemokine receptor, CCR5. Our findings imply that GVHD should be considered in the differential diagnosis of noninfectious angiitis-like disease of the CNS in long-term survivors after allogeneic BMT. Infiltrating cells, in analogy to typical target organs of GVHD such as skin or liver, expressed CD11a and CCR5. These findings could be of etiopathological, diagnostic and therapeutic relevance.

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Section: Resultssupporting

confidence: 88%

Section: Resultssupporting

confidence: 61%

Section: Introductionmentioning

confidence: 99%

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Cerebral angiitis in four patients with chronic GVHD

Sostak

Eigenbrod

et al. 2009

Bone Marrow Transplant

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“…Of the previously reported cases, there are limited histological data available and variable pathological findings. 1,[3][4][5][6] Figure 1 MRI of the brain demonstrating right parietal lobe lesions.…”

mentioning

confidence: 99%

Central nervous system graft-versus-host disease presenting with granulomatous encephalitis

Kew

Macaulay

Burrell

et al. 2007

Bone Marrow Transplant

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“…Although not one of the main manifestation organs, GVHD may also affect the CNS, even if thought to occur rarely and evidence being limited to single cases (6)(7)(8)(9)(10). Because GVHD of the CNS is difficult to distinguish from other complications such as relapse, infections, and toxicity related to therapy, a thorough characterization of CNS GVHD is challenging (7,11).…”

mentioning

confidence: 99%

Graft versus self (GvS) against T-cell autoantigens is a mechanism of graft–host interaction

Mirza

Zierhut²,

Korn

et al. 2016

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

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Graft-versus-host disease (GVHD) represents the major nonrelapse complication of allogeneic hematopoietic cell transplantation. Although rare, the CNS and the eye can be affected. In this study, manifestation in the retina as part of the CNS and T-cell epitopes recognized by the allogeneic T cells were evaluated. In 2 of 6 patients with posttransplantation retina diseases and 6 of 22 patients without ocular symptoms, antigen-specific T-cell responses against retina-specific epitopes were observed. No genetic differences between donor and recipient could be identified indicating T-cell activation against self-antigens (graft versus self). Transplantation of a preexisting immunity and cross-reactivity with ubiquitous epitopes was excluded in family donors and healthy individuals. In summary, an immunological reaction against retina cells represents a mechanism of graft-versus-host interaction following hematopoietic cell transplantation.

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CNS angiitis in graft vs host disease

Cited by 72 publications

References 8 publications

Cerebral angiitis in four patients with chronic GVHD

Cerebral angiitis in four patients with chronic GVHD

Central nervous system graft-versus-host disease presenting with granulomatous encephalitis

Graft versus self (GvS) against T-cell autoantigens is a mechanism of graft–host interaction

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