Class II MHC antigen presentation defect in neonatal monocytes is not correlated with decreased MHC-II expression

Canaday, David H.; Chakravarti, Soma; Srivastava, Tarun; Tisch, Daniel J.; Cheruvu, Vinay K.; Smialek, Jamie L.; Ramachandra, Lakshmi

doi:10.1016/j.cellimm.2007.01.003

Cited by 23 publications

(19 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The incidence of chronic GVHD after unrelated cord blood (HLA 4-6/6) is lower than seen with matched-unrelated donors but similar to that seen after HLA-identical sibling bone marrow transplantation, about 20% (Eapen et al, 2007). Umbilical cord blood contains a high number of naïve T cells (Garderet et al, 1998) and antigen presentation with cord blood dendritic cells is inefficient, explaining why their potential to cause GVHD is lower (Canaday et al, 2006).…”

Section: Incidence and Risk Factorsmentioning

confidence: 98%

Optimal management of chronic graft‐versus‐host disease in children

Jacobsohn

2010

Br J Haematol

View full text Add to dashboard Cite

SummaryChronic graft-versus-host disease (GVHD) is a major complication after allogeneic haematopoietic stem cell transplantation (HSCT). Not only is it the major cause of late mortality in HSCT patients, but it also accounts for significant morbidity. Much of the literature on chronic GVHD has focused on adults. Chronic GVHD is of major importance in children, especially since they have years to live following the complications of chronic GVHD and its therapy. The goal is to review incidence, manifestations, and therapies, especially when applicable to the paediatric population.

show abstract

Section: Incidence and Risk Factorsmentioning

confidence: 98%

Optimal management of chronic graft‐versus‐host disease in children

Jacobsohn

2010

Br J Haematol

View full text Add to dashboard Cite

show abstract

“…Cells were stimulated in the presence or absence of M. tuberculosis or its fractions for 48 h, when IL-2 and proliferation were measured. Supernatants from activated CD4 ϩ T cells were assayed for IL-2 production using a set of capture and detection MAbs from eBioscience previously described (11). Briefly, diluted supernatants were added to Immulon 4HBX flat-bottom microtiter plates (Thermo) coated with purified IL-2 MAb (1 g/ml).…”

Section: Assays Of Cd4mentioning

confidence: 99%

Mycobacterium tuberculosisCell Wall Glycolipids Directly Inhibit CD4⁺T-Cell Activation by Interfering with Proximal T-Cell-Receptor Signaling

et al. 2009

Self Cite

View full text Add to dashboard Cite

Immune evasion is required for Mycobacterium tuberculosis to survive in the face of robust adaptive CD4؉ T-cell responses. We have previously shown that M. tuberculosis can indirectly inhibit CD4 ؉ T cells by suppressing the major histocompatibility complex class II antigen-presenting cell function of macrophages. This study was undertaken to determine if M. tuberculosis could directly inhibit CD4 ؉ T-cell activation. Murine CD4 ؉ T cells were purified from spleens by negative immunoaffinity selection followed by flow sorting. Purified CD4 ؉ T cells were activated for 16 to 48 h with CD3 and CD28 monoclonal antibodies in the presence or absence of M. tuberculosis and its subcellular fractions. CD4؉ T-cell activation was measured by interleukin 2 production, proliferation, and expression of activation markers, all of which were decreased in the presence of M. tuberculosis. Fractionation identified that M. tuberculosis cell wall glycolipids, specifically, phosphatidylinositol mannoside and mannosecapped lipoarabinomannan, were potent inhibitors. Glycolipid-mediated inhibition was not dependent on Toll-like receptor signaling and could be bypassed through stimulation with phorbol 12-myristate 13-acetate and ionomycin. ZAP-70 phosphorylation was decreased in the presence of M. tuberculosis glycolipids, indicating that M. tuberculosis glycolipids directly inhibited CD4؉ T-cell activation by interfering with proximal T-cell-receptor signaling.Aerosolized Mycobacterium tuberculosis infects alveolar and lung parenchymal macrophages, where it replicates unrestrained in the face of innate responses until T-cell immunity controls its growth. Despite robust activation of innate and adaptive immunity, M. tuberculosis survives and persists as a latent infection (15, 18). CD4 ϩ T cells have a central role in controlling M. tuberculosis during acute and latent infections (53). Animal studies have shown that depletion or absence of CD4 ϩ T cells during primary infection results in unchecked M. tuberculosis growth in the lung and decreased survival (37,38,41). Depletion of CD4 ϩ T cells during latent infection also worsens disease and survival (46). In humans, loss of CD4 ϩ T cells from progressive human immunodeficiency virus infection is directly responsible for the high rates of tuberculosis in human immunodeficiency virus-infected persons (48).Much is known about how M. tuberculosis manipulates macrophages for its survival (19,29,44). However, the way in which M. tuberculosis interferes with adaptive T-cell immunity is not well understood. Our recent studies have demonstrated that M. tuberculosis can modulate CD4 ϩ T-cell function both indirectly and directly. M. tuberculosis, through Toll-like receptor 2 (TLR-2), inhibits gamma-interferon-regulated genes that result in decreased major histocompatibility complex class II (MHC-II) antigen processing by macrophages for effector and memory CD4 ϩ T cells (22,23,40,43). M. tuberculosis can also induce increased adhesion to fibronectin through ␣ 5 ␤ 1 integrin on CD4 ϩ T cells (45)...

show abstract

“…The most comprehensive study of MHC II antigen processing and presentation function in neonates was performed using cord blood-derived monocytes as APC. Here, a defect in the presentation, but not in the processing of MHC II antigens was demonstrated [15]. To the best of our knowledge, no report exists on the ability of human neonatal DC to process and present antigen via the MHC class I pathway.…”

Section: Discussionmentioning

confidence: 79%

Human Neonatal Dendritic Cells Are Competent in MHC Class I Antigen Processing and Presentation

et al. 2007

View full text Add to dashboard Cite

Neonates are clearly more susceptible to severe disease following infection with a variety of pathogens than are adults. However, the causes for this are unclear and are often attributed to immunological immaturity. While several aspects of immunity differ between adults and neonates, the capacity of dendritic cells in neonates to process and present antigen to CD8+ T cells remains to be addressed. We used human CD8+ T cell clones to compare the ability of neonatal and adult monocyte-derived dendritic cells to present or process and present antigen using the MHC class I pathway. Specifically, we assessed the ability of dendritic cells to present antigenic peptide, present an HLA-E–restricted antigen, process and present an MHC class I-restricted antigen through the classical MHC class I pathway, and cross present cell-associated antigen via MHC class I. We found no defect in neonatal dendritic cells to perform any of these processing and presentation functions and conclude that the MHC class I antigen processing and presentation pathway is functional in neonatal dendritic cells and hence may not account for the diminished control of pathogens.

show abstract

Class II MHC antigen presentation defect in neonatal monocytes is not correlated with decreased MHC-II expression

Cited by 23 publications

References 41 publications

Optimal management of chronic graft‐versus‐host disease in children

Optimal management of chronic graft‐versus‐host disease in children

Mycobacterium tuberculosisCell Wall Glycolipids Directly Inhibit CD4⁺T-Cell Activation by Interfering with Proximal T-Cell-Receptor Signaling

Human Neonatal Dendritic Cells Are Competent in MHC Class I Antigen Processing and Presentation

Contact Info

Product

Resources

About

Class II MHC antigen presentation defect in neonatal monocytes is not correlated with decreased MHC-II expression

Cited by 23 publications

References 41 publications

Optimal management of chronic graft‐versus‐host disease in children

Optimal management of chronic graft‐versus‐host disease in children

Mycobacterium tuberculosisCell Wall Glycolipids Directly Inhibit CD4+T-Cell Activation by Interfering with Proximal T-Cell-Receptor Signaling

Human Neonatal Dendritic Cells Are Competent in MHC Class I Antigen Processing and Presentation

Contact Info

Product

Resources

About

Mycobacterium tuberculosisCell Wall Glycolipids Directly Inhibit CD4⁺T-Cell Activation by Interfering with Proximal T-Cell-Receptor Signaling