B Cells Are Required for Generation of Protective Effector and Memory CD4 Cells in Response to <i>Pneumocystis</i> Lung Infection

Lund, Frances E.; Hollifield, Melissa; Schuer, Kevin M.; Lines, J. Louise; Randall, Troy D.; Garvy, Beth A.

doi:10.4049/jimmunol.176.10.6147

Cited by 166 publications

(167 citation statements)

References 27 publications

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“…muris through antigen presentation to CD4 T cells [20]. B cells seem to be required for the generation of CD4 effector cells capable of migrating to the lungs as well as for the expansion and generation of memory CD4 cells [20]. In order to identify the risk of PCP due to RTX, we reviewed the literature in patients with haematological malignancies, solid-organ transplantation and AAV.…”

Section: Discussionmentioning

confidence: 99%

Should Pneumocystis jiroveci prophylaxis be recommended with Rituximab treatment in ANCA-associated vasculitis?

Besada

Nossent

2013

Clin Rheumatol

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Reports in haematology, transplantation medicine and rheumatology indicate that Rituximab, a B cell depleting therapy, increases the risk for Pneumocystis jiroveci pneumopathy. Patients with ANCA-associated vasculitis have an increased incidence of Pneumocystis jiroveci pneumopathy compared to other autoimmune diseases and Rituximab is often used to induce and maintain remission.Herein we present a case of a patient with granulomatosis with polyangiitis treated with Rituximab for relapse that developed Pneumocystis jiroveci pneumopathy 3 months after and we review the relevant literature to assess Pneumocystis jiroveci pneumopathy incidence and risks factors under Rituximab. We also discuss whether pneumocystis jiroveci screening before Rituximab and Pneumocystis jiroveci pneumopathy prophylaxis under Rituximab are indicated.Pneumocystis jiroveci colonization is found in 25% of patients with autoimmune diseases. However the association between colonization and Pneumocystis jiroveci pneumopathy development is not very strong.Pneumocystis jiroveci pneumopathy incidence in ANCA-associated vasculitis patients treated with Rituximab is found to be 1.2%. Therefore evidence and practice do not support the use of Pneumocystis jiroveci pneumopathy chemoprophylaxis in all ANCA-associated vasculitis patients receiving Rituximab. CD4 cell count cut-off does not work well in patients treated with Rituximab as it does not reflect T-cell impairment following B cell depletion.To help stratify the risk of both colonization and Pneumocystis jiroveci pneumopathy development, assessment of the patient's net stat of immunodeficiency before administering Rituximab -including age, renal or lung involvement, previous infections due to T cell dysfunction, blood tests (lymphocytopenia, low CD4 cell count) and concomitant therapy -is warranted.

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Section: Discussionmentioning

confidence: 99%

Should Pneumocystis jiroveci prophylaxis be recommended with Rituximab treatment in ANCA-associated vasculitis?

Besada

Nossent

2013

Clin Rheumatol

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“…A T-sejtek kb. 6%-án kimutatható CD20 expresszió [10], és a memóra típusú CD4 + Tsejtek kialakulásában, érésében a B-sejtek antigén prezentálásának is valószínű a szerepe [11].…”

Section: Ezek Alapján Határoztuk El Hogy Felmérjük a Klinikánkon 200unclassified

“…Az opportunista fertőzés leküzdésében kiemelkedő szerepe van a CD4 + sejteknek, hiszen ezek a nyirokcsomókban találkoznak az antigénprezentáló sejtekkel, majd a tüdőbe vándorolva aktiválják a macrophagokat, és elősegítik a B-sejtek antitest termelését is, ami szintén fokozza a P. jirovecii fagocitózisát. A PCP leküzdése tehát alapvetően T-sejt dependens folyamat [11]. Ugyanakkor megfigyelték, hogy a naív T-sejtek hatékony effektor sejté történő differenciálódásához és a CD4 + memória típusú T-sejtek kialakulásához B-sejtek szükségesek, azoknak antigén prezentáló szerepük lehet a T-sejtek felé [11].…”

Section: Progresszív Multifokális Leukoencephalopathia (Pml)unclassified

“…A PCP leküzdése tehát alapvetően T-sejt dependens folyamat [11]. Ugyanakkor megfigyelték, hogy a naív T-sejtek hatékony effektor sejté történő differenciálódásához és a CD4 + memória típusú T-sejtek kialakulásához B-sejtek szükségesek, azoknak antigén prezentáló szerepük lehet a T-sejtek felé [11]. Esetismertetésekben beszámoltak arról is, hogy a PCP rizikója fokozott volt X-hez kötött agammaglobulinaemiában is [28], tehát a PCP leküzdése nem csak a CD4 + T-sejtek, hanem az egész immunrendszer feladata.…”

Section: Progresszív Multifokális Leukoencephalopathia (Pml)unclassified

“…Esetismertetésekben beszámoltak arról is, hogy a PCP rizikója fokozott volt X-hez kötött agammaglobulinaemiában is [28], tehát a PCP leküzdése nem csak a CD4 + T-sejtek, hanem az egész immunrendszer feladata. Több irodalmi adat utal arra, hogy rituximab kezelés mellett a a PCP kialakulásának rizikója fokozottabb lehet [11,[27][28][29]. Ausztrál szerzők az R-CHOP14 (időintenzifikált, 14 napos ciklusokban alkalmazott kezelés) terápia mellett retrospektív vizsgálatuk során a PCP rizikóját 10%-osnak találták, így ezekben az esetekben a sulfamethoxazole+timethoprim profilaxis alkalmazását javasolják, két másik vizsgálatban hasonló, 10-15%-os PCP előfordulásról számoltak be 32, illetve 50 beteg adatait áttekintve [27].…”

Section: Progresszív Multifokális Leukoencephalopathia (Pml)unclassified

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Antigen Presentation in Transplantation

Oberbarnscheidt¹,

Lakkis²

2010

Immunotherapy in Transplantation

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Transplantation of solid organs between genetically distinct individuals leads, in the absence of immunosuppression, to T cell-dependent transplant rejection. Activation of graft-reactive T cells relies on the presentation of transplant-derived antigens (intact donor MHC molecules or processed peptides on host MHC molecules) by mature dendritic cells (DCs). This review will focus on novel insights regarding the steps for maturation and differentiation of DCs that are necessary for productive presentation of transplant antigens to host T cells. These steps include the licensing of DCs by the microbiota, their activation and maturation following recognition of allogeneic non-self and their capture of donor cell exosomes to amplify presentation of transplant antigens. Recent Advances on Innate Immunity in TransplantationTransplantation of organs from cadaveric or living donors can cure end-stage organ failure in transplant recipients. However, with the exception of organ donation between identical twins, transplantation sets up a cascade of inflammatory events leading to recognition of the allograft (see Glossary) by the host's immune system and to T cell-dependent transplant rejection. To prevent rejection, transplant patients take global immunosuppressive medications lifelong, which can lead to side effects as well as increased susceptibility to infections and malignancies. In order to develop more specific and less toxic therapies, a better understanding of the steps leading to robust activation of alloreactive T cells by innate immune cells is required. To this end, a large body of work has focused on the biology of alloreactive T cells and approaches to delete or suppress them. In recent years, several groups have turned their attention to the antigen-presenting cells (APCs) that initiate the activation of allogeneic T cells, revealing at least 3 new mechanisms by which innate Correspondence: malegre@midway.uchicago.edu (M.L. Alegre). Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. immunity controls the quality and robustness of alloreactive T cell priming (Figure 1). First, the composition of the microbiota within the donor and the host prior to transplantation was shown to tune the capacity of APCs to prime alloreactive T cells and dictate the subsequent kinetics of graft rejection. Second, following transplantation, recognition by recipient mononuclear phagocytes of non-self determinants in the donor graft, encoded by non-MHC genes, was found to promote maturation and differentiation of these cells enhancing subsequent priming of alloreactive T cells. Third, ...

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B Cells Are Required for Generation of Protective Effector and Memory CD4 Cells in Response to Pneumocystis Lung Infection

Cited by 166 publications

References 27 publications

Should Pneumocystis jiroveci prophylaxis be recommended with Rituximab treatment in ANCA-associated vasculitis?

Should Pneumocystis jiroveci prophylaxis be recommended with Rituximab treatment in ANCA-associated vasculitis?

Immunological changes in diffuse large B-cell lymphomas after Rituximab-CHOP treatment: Own data and review of the literature

Antigen Presentation in Transplantation

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