Abnormalities in subset distribution, activation, and differentiation of T ceils isolated from large intestine biopsies in HIV infection

Schneider, Thomas; Ullrich, Reiner; Bergs, C; Schmidt, Wolfgang; Riecken, E. O.; Zeitz, Martin

doi:10.1111/j.1365-2249.1994.tb07014.x

Cited by 56 publications

(15 citation statements)

References 29 publications

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“…CD103 expression was high in the cervix, consistent with its mucosal nature. We did not find changes in CD103 expression in HIV-infected patients, unlike Schneider et al, 23 who found decreased CD103 expression on intestinal CD8 T cells, although not on CD4 cells, of HIV-infected patients. The fact that our data were based on all CD3 cells may explain this difference.…”

Section: Discussioncontrasting

confidence: 98%

T-Lymphocyte Profile and Total and Virus-Specific Immunoglobulin Concentrations in the Cervix of HIV-1-Infected Women

Quayle

Kourtis²,

Cu‐Uvin³

et al. 2007

JAIDS Journal of Acquired Immune Deficiency Syndromes

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Section: Discussioncontrasting

confidence: 98%

T-Lymphocyte Profile and Total and Virus-Specific Immunoglobulin Concentrations in the Cervix of HIV-1-Infected Women

Quayle

Kourtis²,

Cu‐Uvin³

et al. 2007

JAIDS Journal of Acquired Immune Deficiency Syndromes

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“…It is not unlikely that the classification of Tregs by an arbitrary cut-off point for the definition of CD25 high cells could result in diverse findings, since CD25 expression is not restricted to regulatory CD4 ϩ cells. 22,36 Moreover, low CD4 ϩ T-cell numbers can make it extremely difficult to set the cut-off for the CD25 high cell population.…”

Section: Discussionmentioning

confidence: 99%

“…22 Biopsies were washed once in 20 mL NaCl 0.9% to remove adherent blood and mucus and cut into small fragments. Fragments were preincubated overnight at 4°C in 50 mL RPMI 1640 medium (Gibco, Karlsruhe, Germany) containing 10% fetal calf serum (FCS), 100 U/mL penicillin, 100 g/mL streptomycin, 50 g/mL gentamycin, 2.5 g/mL amphotericin, 25 mM HEPES buffer (all from Seromed Biochrom, Berlin, Germany), 0.05 M 2-mercaptoethanol (Gibco), 0.01% collagenase (CLS III; Seromed Biochrom), 0.01% trypsin inhibitor (type I-S; Sigma-Aldrich, Steinheim, Germany), and 0.01% DNAse (DNAse I from bovine pancreas; Hoffmann-La Roche, Basel, Switzerland) and then incubated for 4 hours (37°C) in a humid chamber (5% CO 2 ).…”

Section: Isolation Of Lamina Propria Mononuclear Cellsmentioning

confidence: 99%

Mucosal FOXP3+ regulatory T cells are numerically deficient in acute and chronic GvHD

Rieger

Loddenkemper

Maul

et al. 2006

Blood

220

144

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CD4 ؉ CD25 ؉ regulatory T cells (Tregs) control immune responses to self-and foreign antigens and play a pivotal role in autoimmune diseases, infectious and noninfectious inflammation, and graft rejection. Since recent experimental studies have indicated that Tregs were able to ameliorate graft-versus-host disease (GvHD), we analyzed the number of infiltrating Tregs in the intestinal mucosa as one site of GvH reactivity using immunoenzymatic labeling to enumerate IntroductionDespite the prophylactic use of potent immunosuppressants, severe graft-versus-host disease (GvHD) is-besides infections-the most relevant complication after allogeneic stem cell transplantation. Immunologically, acute GvHD is characterized by an expansion of donor lymphocytes with cytotoxic reactivity against recipient histocompatibility antigens. The resulting clinical picture includes life-threatening destruction of skin, gut, and liver tissue.In acute GvHD, the transferred immune system lacks the capability to gain control over alloreactive T-cell clones. Therefore, the understanding of mechanisms by which an organism controls allo-or autoimmune reactivity is crucial for the development of successful strategies to prevent and/or control GvHD. Recently, these mechanisms have been further elucidated by the description of a distinct CD4 ϩ T-cell population with the capability to confer nonresponsiveness to T cells against autologous and allogeneic antigens. [1][2][3] These suppressor or regulatory T cells were originally described as a lymphocyte subset that prevents autoimmunity caused by neonatal thymectomy in mice 1 and are characterized by the expression of the interleukin-2 (IL-2) receptor ␣-chain (CD25). More recently, FOXP3, which encodes for a forkhead/winged helix transcription factor called Scurfin, has been identified to be a key regulatory gene required for the development and functional activity of regulatory T cells. [4][5][6][7] Tregs are able to suppress CD4 ϩ and CD8 ϩ T-cell responses to auto-and alloantigens in a contactdependent fashion. 8 In animal models, they can prevent graft rejection 2,3,9 and autoimmune diseases, 8,10 and there is also evidence that inappropriate numbers of Tregs may contribute to the development of chronic inflammatory diseases. 11 Consequently, the question has been raised whether Tregs are also capable of suppressing GvHD. Indeed, it has been shown in different murine models that freshly isolated or ex vivo-expanded donor-type CD4 ϩ CD25 ϩ Tregs are able to delay or even prevent GvH reactivity. [12][13][14][15] Consistent with this, the selective depletion of Tregs leads to an increased severity of acute GvHD in vivo. 16 In humans, however, available data are ambiguous. Whereas Clark et al found elevated numbers of CD4 ϩ CD25 high cells in the peripheral blood of patients with chronic GvHD, 17 Miura et al observed a significantly decreased FOXP3 mRNA expression in the peripheral blood of patients suffering from allogeneic or autologous GvHD. 18 Since the presence of Tregs in the peripheral blo...

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“…Although there are methodologic constraints in this approach, including variation in the exact site of biopsy or resection and the small area of colon assessed in both the HIV-infected (median ϭ 0.99/mm 2 ) and control samples (median ϭ 1.54/mm 2 ), our results were consistent with those of others which suggest an overall increase in CD8 ϩ T-cell numbers in the gut during HIV infection. 1,3,4,32 Overall, despite the clear loss of CD161 ϩϩ /MAIT cells from blood, they are still detectable in gut, as judged by analysis of CD8 ϩ CD3 ϩ MDR1 ϩϩ cells. …”

mentioning

confidence: 99%

Early and nonreversible decrease of CD161++/MAIT cells in HIV infection

Cosgrove

Ussher

Rauch

et al. 2013

Blood

279

364

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Key Points• The frequency of CD161 ϩϩ MAIT cells is dramatically decreased in the blood of HIVinfected patients, and they are nonrecoverable with HAART.• Gut sequestration and apoptosis in response to bacterial signals may, amongst others, be mechanisms that contribute to this. IntroductionThe natural course of human immunodeficiency virus type 1 (HIV-1) infection is associated with progressive immune dysfunction, perturbation of immune-cell subsets and increased opportunistic infections. In early disease, there is a dramatic loss of CD4 ϩ T cells from the gastrointestinal tract resulting in impaired mucosal immunity, reduced peripheral CD4 ϩ T-cell count, and increased systemic T-cell activation. [1][2][3][4] These factors contribute to an increased susceptibility to infection with specific organisms such as Mycobacterium tuberculosis and Candida albicans. [5][6][7] In addition, more recent evidence suggests an important role for the loss of CD8 ϩ T cells in susceptibility to bacterial pneumonia and all-cause mortality in HIV infection. 8 MAIT cells are a distinct subset of tissue-infiltrating lymphocytes with antibacterial functions that account for up to one-third of the CD8 ϩ T-cell population in the blood of healthy individuals. [9][10][11] MAIT cells are identified by expression of a semi-invariant T-cell receptor (TCR), iV␣7.2, 10,12,13 which recognizes ligands presented by MHC class I related (MR1) protein. 14 MR1 presentation occurs on dendritic cells, monocytes, and lung epithelial cells in response to bacterial pathogens. 9,10,12 MAIT cells are activated in vitro in an MR1-dependent fashion by a range of bacterial and fungal pathogens, including Escherichia coli, M tuberculosis, and C albicans, 9,10 and in mouse models have been shown to provide protection against bacterial infection. 10,15 In addition, MAIT cells have been shown to be lost from the blood and present in the lungs of patients with active tuberculosis, suggesting they may play an important role in host immunity to M tuberculosis. 9,10 Specific subsets of CD4 ϩ and CD8 ϩ T cells, termed Th17 and Tc17, are defined by their ability to produce IL17A and are important in the regulation of mucosal integrity and antibacterial immunity. [16][17][18][19][20] Early in HIV infection, Th17 cells are lost from the gastrointestinal tract, but may be restored through long-term highly active antiretroviral therapy (HAART) concurrent with a reduction in immune activation levels. 21 The loss of this IL17A and Submitted June 12, 2012; accepted November 26, 2012. Prepublished online as Blood First Edition paper, December 18, 2012; DOI 10.1182 DOI 10. /blood-2012 *C.C. and J.E.U. contributed equally to this work.The online version of this article contains a data supplement.The publication costs of this article were defrayed in part by page charge payment. Therefore, and solely to indicate this fact, this article is hereby marked ''advertisement'' in accordance with 18 USC section 1734. For personal use only. on May 7, 2018. by guest www.bloodjournal.org...

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Abnormalities in subset distribution, activation, and differentiation of T ceils isolated from large intestine biopsies in HIV infection

Cited by 56 publications

References 29 publications

T-Lymphocyte Profile and Total and Virus-Specific Immunoglobulin Concentrations in the Cervix of HIV-1-Infected Women

T-Lymphocyte Profile and Total and Virus-Specific Immunoglobulin Concentrations in the Cervix of HIV-1-Infected Women

Mucosal FOXP3+ regulatory T cells are numerically deficient in acute and chronic GvHD

Early and nonreversible decrease of CD161++/MAIT cells in HIV infection

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