Impaired T Cell Stimulation And Lipid Antigen Presentation By Pulmonary, But Not Systemic, CD11c+ Antigen-Presenting Cells In Cystic Fibrosis

2012 ◽  
Author(s):  
Yaqin Xu ◽  
Anja Krause ◽  
Tilla Worgall ◽  
Maria Limberis ◽  
Stefan Worgall
Keyword(s):  
Cystic Fibrosis ◽  
T Cell ◽  
Antigen Presentation ◽  
Antigen Presenting Cells ◽  
Cell Stimulation ◽  
T Cell Stimulation ◽  
Lipid Antigen ◽  
Antigen Presenting

scholarly journals Abortive Proliferation of Rare T Cells Induced by Direct or Indirect Antigen Presentation by Rare B Cells In Vivo

1998 ◽  
Vol 187 (10) ◽  
pp. 1611-1621 ◽  
Author(s):  
Sarah E. Townsend ◽  
Christopher C. Goodnow
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
Antigen Presentation ◽  
Cell Fate ◽  
T Cell Activation ◽  
Cell Activation ◽  
Antigen Presenting Cells ◽  
Antigen Presenting

Antigen-specific B cells are implicated as antigen-presenting cells in memory and tolerance responses because they capture antigens efficiently and localize to T cell zones after antigen capture. It has not been possible, however, to visualize the effect of specific B cells on specific CD4+ helper T cells under physiological conditions. We demonstrate here that rare T cells are activated in vivo by minute quantities of antigen captured by antigen-specific B cells. Antigen-activated B cells are helped under these conditions, whereas antigen-tolerant B cells are killed. The T cells proliferate and then disappear regardless of whether the B cells are activated or tolerant. We show genetically that T cell activation, proliferation, and disappearance can be mediated either by transfer of antigen from antigen-specific B cells to endogenous antigen-presenting cells or by direct B–T cell interactions. These results identify a novel antigen presentation route, and demonstrate that B cell presentation of antigen has profound effects on T cell fate that could not be predicted from in vitro studies.

Generation of Anti-Leukemia Reactive T-Cells by Costimulation with Established B-ALL Cell Lines Expressing Costimulatory Molecules.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1094-1094
Author(s):  
Ying Yan ◽  
Peter Steiherz ◽  
Jianda Ruan ◽  
Yibang Chen ◽  
Sunil Abhyankar ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cell ◽  
Cell Lines ◽  
Costimulatory Molecules ◽  
Cell Phenotype ◽  
Cell Stimulation ◽  
T Cell Stimulation ◽  
B7 Family ◽  
Antigen Presenting

Abstract Activated B cells expressing the B7 family of molecules are efficient antigen presenting cells. However, most of B-lineage leukemia cells do not fullfill these criteria, having lost their immunostimulatory potential both in vivo and in vitro. We have established 3 human B-ALL(L3) cell-lines (BA-25, BA-78 and BA91) which in comparison with an established pre-B-ALL cell line (BA-127) and other patients-derived pre-B-ALL blast cells do express the costimulatory molecules CD80 and/or CD86, as well as other critical costimulatory molecules for T-cell stimulation such as: CD40, ICAM-I, LFA-3 and CD72. Flow cytometry analysis demonstrate that these B-ALL cells have an activated B-cell phenotype (CD19+, CD20+, CD22+, CD38+, CD71+, CD75+, DR+, HLA-class-I and HLA-class-II). Chromosomal translocations consistent with B-ALL (L3) were determined in BA-25 [t(2;28)(p12;q24)], BA-78 [t(8;14)(q24,q32)] and BA-91 [t(8;14) (q24,q32)]. No EBV DNA sequence was found in these B-ALL cell lines by Southern blot analysis with a probe for EBV genome. In mixted lymphocyte reaction (MLR) assay, Allogeneic T cells were stimulated by BA-25 and BA-91 cells at a B : T cells ratios of 1/30, 1/100, 1/300 and 1/1000. The BA-25 and BA-91 demonstrated 1-2 logs higher ccpm than the control pre-B-ALL cells (BA-127) which with no expression of B7 family molecules. The dose response curves for the B-cell mixture ratio display a linear pattern between 217-213 log2 ccpm. To determine T cell stimulation potential of the B-ALL cells, we co-cultured allogeneic PBMC with irradiated (3,000 Rad x-ray) BA-25 cells at 30:1 effector/stimulator ratio and achieved a 3–4 fold expansion of T cells after one round 7-day stimulation. Stimulation of allogeneic PBMC with BA-25 elicited proliferation of the T-cells and lysis of BA-25 as an target in a 4h Cr51 release assay, demonstrating BA-25 as an antigen presenting cell. Studies also show that the BA-25 cells could stimulate allo-cytolytic reactions by CTLs against other human leukemic target cells which lack these molecules and fail to stimulate T cell responses by themselves. Thus, BA-25 and other similar lines may prove useful for the provision of costimulatory signal needed to stimulate T-cell response against leukemias lacking these molecules.

Class II MHC/Peptide Complexes on T Cell Antigen-Presenting Cells: Agonistic Antigen Recognition Inhibits Subsequent Antigen Presentation

1998 ◽  
Vol 186 (2) ◽  
pp. 111-120 ◽  
Author(s):  
Mark D. Mannie ◽  
John P. Nardella ◽  
Gregory A. White ◽  
Paula Y. Arnold ◽  
Daniel K. Davidian
Keyword(s):  
T Cell ◽  
Antigen Presentation ◽  
Antigen Presenting Cells ◽  
Class Ii ◽  
Antigen Recognition ◽  
Cell Antigen ◽  
Class Ii Mhc ◽  
Peptide Complexes ◽  
Antigen Presenting

Indirect inhibition of in vivo and in vitro T-cell responses by intravenous immunoglobulins due to impaired antigen presentation

Blood ◽  
2010 ◽  
Vol 115 (9) ◽  
pp. 1727-1734 ◽  
Author(s):  
Éric Aubin ◽  
Réal Lemieux ◽  
Renée Bazin
Keyword(s):  
T Cell ◽  
Antigen Presentation ◽  
T Cell Activation ◽  
T Cell Responses ◽  
Antigen Presenting Cells ◽  
In Vivo Model ◽  
Cell Responses ◽  
Antigen Presenting

Abstract Several clinical studies done with intravenous immunoglobulin (IVIg)–treated autoimmune patients as well as several in vitro studies have revealed that IVIg can reduce polyclonal T-cell activation and modify their cytokine secretion pattern. However, their effect on (auto)antigen-specific T-cell responses has never been addressed directly. In the present work, we used an in vivo model of induction of antigen-specific T-cell responses and an in vitro antigen presentation system to study the effects of IVIg on T-cell responses. The results obtained showed that IVIg inhibited both the in vivo and in vitro antigen-specific T-cell responses but that this effect was the indirect consequence of a reduction in the antigen presentation ability of antigen-presenting cells. The inhibitory effect of IVIg was FcγRIIb-independent, suggesting that IVIg must interfere with activating FcγRs expressed on antigen-presenting cells to reduce their ability to present antigens. Such inhibition of T-cell responses by reducing antigen presentation may therefore contribute to the well-known anti-inflammatory effects of IVIg in autoimmune diseases.

scholarly journals High Level Expression of MHC-II in HPV+ Head and Neck Cancers Suggests that Tumor Epithelial Cells Serve an Important Role as Accessory Antigen Presenting Cells

Cancers ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1129 ◽  
Author(s):  
Steven F. Gameiro ◽  
Farhad Ghasemi ◽  
John W. Barrett ◽  
Anthony C. Nichols ◽  
Joe S. Mymryk
Keyword(s):  
T Cell ◽  
Epithelial Cells ◽  
Antigen Presentation ◽  
Head And Neck ◽  
Antigen Presenting Cells ◽  
Human Papillomaviruses ◽  
Mhc Ii ◽  
Hpv Status ◽  
Antigen Presenting ◽  
The Impact

High-risk human papillomaviruses (HPVs) are responsible for a subset of head and neck squamous cell carcinomas (HNSCC). Expression of class II major histocompatibility complex (MHC-II) is associated with antigen presenting cells (APCs). During inflammation, epithelial cells can be induced to express MHC-II and function as accessory APCs. Utilizing RNA-seq data from over 500 HNSCC patients from The Cancer Genome Atlas, we determined the impact of HPV-status on the expression of MHC-II genes and related genes involved in their regulation, antigen presentation, and T-cell co-stimulation. Expression of virtually all MHC-II genes was significantly upregulated in HPV+ carcinomas compared to HPV− or normal control tissue. Similarly, genes that encode products involved in antigen presentation were also significantly upregulated in the HPV+ cohort. In addition, the expression of CIITA and RFX5—regulators of MHC-II—were significantly upregulated in HPV+ tumors. This coordinated upregulation of MHC-II genes was correlated with higher intratumoral levels of interferon-gamma in HPV+ carcinomas. Furthermore, genes that encode various co-stimulatory molecules involved in T-cell activation and survival were also significantly upregulated in HPV+ tumors. Collectively, these results suggest a previously unappreciated role for epithelial cells in antigen presentation that functionally contributes to the highly immunogenic tumor microenvironment observed in HPV+ HNSCC.

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