We are analyzing https://link.springer.com/article/10.1007/s10620-009-0839-8.

Title:
Refractory Colitis Following Anti-CTLA4 Antibody Therapy: Analysis of Mucosal FOXP3+ T Cells | Digestive Diseases and Sciences
Description:
Ipilimumab is a humanized antibody to CTLA4 and is used to treat cancers refractory to conventional treatment. We treated 21 patients with refractory melanoma or prostate cancer with anti-CTLA4 antibody (ipilimumab), with subsequent development of significant colitis in nine cases. Two of these nine did not respond rapidly to high-dose (2 mg kg−1 day−1) glucocorticoids or infliximab. They required additional immunosuppression, and one ultimately died of opportunistic infection, representing a more refractory course than has previously been described complicating ipilimumab therapy. Both patients had received radiation to the pelvis for prostate cancer less than 1 year prior to receiving ipilimumab. We performed immunohistochemical analysis of colon biopsies from ipilimumab recipients to determine if colitis correlates with depletion of intramucosal FOXP3+ regulatory T cells (Tregs), which normally express CTLA4. However, we found no evidence of FOXP3+ T cell depletion in any of the nine patients who developed colitis.
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Topics {✒️}

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Inflammatory bowel disease and cancer response due to anti-CTLA-4: is it in the flora?

Schema {🗺️}

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         headline:Refractory Colitis Following Anti-CTLA4 Antibody Therapy: Analysis of Mucosal FOXP3+ T Cells
         description:Ipilimumab is a humanized antibody to CTLA4 and is used to treat cancers refractory to conventional treatment. We treated 21 patients with refractory melanoma or prostate cancer with anti-CTLA4 antibody (ipilimumab), with subsequent development of significant colitis in nine cases. Two of these nine did not respond rapidly to high-dose (2 mg kg−1 day−1) glucocorticoids or infliximab. They required additional immunosuppression, and one ultimately died of opportunistic infection, representing a more refractory course than has previously been described complicating ipilimumab therapy. Both patients had received radiation to the pelvis for prostate cancer less than 1 year prior to receiving ipilimumab. We performed immunohistochemical analysis of colon biopsies from ipilimumab recipients to determine if colitis correlates with depletion of intramucosal FOXP3+ regulatory T cells (Tregs), which normally express CTLA4. However, we found no evidence of FOXP3+ T cell depletion in any of the nine patients who developed colitis.
         datePublished:2009-06-09T00:00:00Z
         dateModified:2009-06-09T00:00:00Z
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            CTLA4
            FOXP3
            Colitis
            Gastroenterology
            Hepatology
            Oncology
            Transplant Surgery
            Biochemistry
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      headline:Refractory Colitis Following Anti-CTLA4 Antibody Therapy: Analysis of Mucosal FOXP3+ T Cells
      description:Ipilimumab is a humanized antibody to CTLA4 and is used to treat cancers refractory to conventional treatment. We treated 21 patients with refractory melanoma or prostate cancer with anti-CTLA4 antibody (ipilimumab), with subsequent development of significant colitis in nine cases. Two of these nine did not respond rapidly to high-dose (2 mg kg−1 day−1) glucocorticoids or infliximab. They required additional immunosuppression, and one ultimately died of opportunistic infection, representing a more refractory course than has previously been described complicating ipilimumab therapy. Both patients had received radiation to the pelvis for prostate cancer less than 1 year prior to receiving ipilimumab. We performed immunohistochemical analysis of colon biopsies from ipilimumab recipients to determine if colitis correlates with depletion of intramucosal FOXP3+ regulatory T cells (Tregs), which normally express CTLA4. However, we found no evidence of FOXP3+ T cell depletion in any of the nine patients who developed colitis.
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      dateModified:2009-06-09T00:00:00Z
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      pageEnd:1405
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         FOXP3
         Colitis
         Gastroenterology
         Hepatology
         Oncology
         Transplant Surgery
         Biochemistry
         general
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      affiliation:
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            address:
               name:Fred Hutchinson Cancer Research Center, Seattle, USA
               type:PostalAddress
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      name:Gideon Steinbach
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            address:
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      name:Fred Hutchinson Cancer Research Center, Seattle, USA
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      name:Fred Hutchinson Cancer Research Center, Seattle, USA
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