scholarly journals Activation of Glomerular Basement Membrane–Specific B Cells in the Renal Draining Lymph Node after T Cell–Mediated Glomerular Injury

2005 ◽  
Vol 16 (11) ◽  
pp. 3256-3263 ◽  
Author(s):  
Julie Robertson ◽  
Jean Wu ◽  
Jon Arends ◽  
Cindy Zhou ◽  
John McMahon ◽  
...  
Keyword(s):  
Lymph Node ◽  
T Cell ◽  
B Cells ◽  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Glomerular Injury ◽  
Draining Lymph Node

scholarly journals Prior Exposure to Ortho-Phthalaldehyde Augments IgE-Mediated Immune Responses to Didecyldimethylammonium Chloride: Potential for 2 Commonly Used Antimicrobials to Synergistically Enhance Allergic Disease

2020 ◽  
Vol 178 (1) ◽  
pp. 127-137
Author(s):  
Hillary L Shane ◽  
Ewa Lukomska ◽  
Lisa Weatherly ◽  
Rachel Baur ◽  
Stacey E Anderson
Keyword(s):  
Lymph Node ◽  
T Cell ◽  
B Cells ◽  
Immune Responses ◽  
Allergic Disease ◽  
Cell Activation ◽  
Immunological Mechanisms ◽  
Draining Lymph Node ◽  
Ige Mediated

Abstract Health-care workers have an increased incidence of allergic disease compared with the general public and are exposed to a variety of high-level disinfectants. Although exposure to these agents has been associated with allergic disease, findings between epidemiology and animal studies often conflict respecting immunological mechanisms. Therefore, we hypothesized that previous exposure to a representative IgE-mediated sensitizer (ortho-phthalaldehyde [OPA]) alters immune responses to a representative T-cell-mediated sensitizer (didecyldimethlyammonium chloride [DDAC]). Here, BALB/c mice were topically exposed to OPA (0.5%) for 3 days, rested, then topically exposed to DDAC (0.0625%, 0.125%, and 0.25%) for 14 days. Coexposure resulted in phenotypic changes in draining lymph node (dLN) cells, including a decreased frequency of CD8+ T cells and increased frequency and number of B cells compared with DDAC-only treated mice. The coexposed mice also had enhanced Th2 responses, including significant alterations in: dLN Il4 (increased), B-cell activation (increased), CD8+ T-cell activation (decreased), and local and systemic IgE production (increased). These changes were not observed if mice were exposed to DDAC prior to OPA. Exposure to OPA alone shows Th2 skewing, indicated by increased activation of skin type 2 innate lymphoid cells, increased frequency and activation of draining lymph node B cells, and increased levels of type 2 cytokines. These findings suggest that the OPA-induced immune environment may alter the response to DDAC, resulting in increased IgE-mediated immune responses. This data may partially explain the discordance between epidemiological and laboratory studies regarding disinfectants and provide insight into the potential immunological implications of mixed chemical exposures.

scholarly journals A MOUSE B-CELL ALLOANTIGEN DETERMINED BY GENE(S) LINKED TO THE MAJOR HISTOCOMPATIBILITY COMPLEX

1973 ◽  
Vol 138 (6) ◽  
pp. 1289-1304 ◽  
Author(s):  
David H. Sachs ◽  
James L. Cone
Keyword(s):  
Major Histocompatibility Complex ◽  
Lymph Node ◽  
T Cell ◽  
B Cells ◽  
Cell Surface ◽  
B Cell ◽  
Surface Antigen ◽  
Major Histocompatibility ◽  
Spleen Cells ◽  
Histocompatibility Complex

Antibodies cytotoxic for only a subpopulation of C57Bl/10 lymph node and spleen cells were detected when rat antiserum against B10.D2 was exhaustively absorbed with B10.A lymphocytes. Antibodies of similar specificity were also detected in B10.A anti-B10.D2 and in B10.A anti-C57Bl/10 alloantisera. Reactions with recombinant strains of mice indicate that the cell-surface antigen(s) responsible for this specificity is determined by gene(s) in or to the left of the Ir-1 region of the major histocompatibility complex. A variety of criteria implicate B cells as the subpopulation of lymphocytes bearing this antigen. In view of these data and the recent report by others of a T-cell alloantigen determined by gene(s) in the major histocompatibility complex, it seems possible that there may be a variety of H-2-linked alloantigens expressed preferentially on subclasses of lymphocytes.

scholarly journals Th2 responses induce humorally mediated injury in experimental anti-glomerular basement membrane glomerulonephritis.

1997 ◽  
Vol 8 (7) ◽  
pp. 1101-1108 ◽  
Author(s):  
X R Huang ◽  
S R Holdsworth ◽  
P G Tipping
Keyword(s):  
T Cells ◽  
T Cell ◽  
Basement Membrane ◽  
Immune Responses ◽  
Glomerular Basement Membrane ◽  
Acute Injury ◽  
Delayed Type Hypersensitivity ◽  
Acute Glomerulonephritis ◽  
Neutrophil Influx ◽  
Mouse Immunoglobulin

Acute autologous phase anti-glomerular basement membrane glomerulonephritis was compared in Th1-prone (C57BL/6) and Th2-prone (BALB/c) mice. Sensitized BALB/c mice, given a subnephritogenic intravenous dose of anti-mouse glomerular basement membrane globulin, developed acute glomerulonephritis characterized by marked proteinuria and glomerular deposition of mouse immunoglobulin and complement. A significant glomerular neutrophil influx was observed, but few T cells and macrophages were present. C57BL/6 mice, given the same dose of disease-inducing globulin, also developed acute glomerulonephritis, although their proteinuria was significantly less. Glomerular deposition of mouse immunoglobulin and complement and the influx of neutrophils were also significantly less than in BALB/c mice. However, their glomerular accumulation of macrophages and T cells was significantly greater. Complement depletion attenuated neutrophil influx and proteinuria in BALB/c mice but did not affect T cell or macrophage accumulation or proteinuria in C57BL/6 mice. CD4+ T cell depletion significantly reduced glomerular macrophage, T cell influx, and proteinuria in C57BL/6 mice, but had no effect on proteinuria or neutrophil influx in BALB/c mice. Thus, immune responses to planted glomerular antigens in Th2-prone mice induce acute injury as a result of antibody deposition, complement activation, and neutrophil influx, whereas immune responses to the same antigen in Th1-prone mice induce delayed-type hypersensitivity-like lesions in affected glomeruli.

scholarly journals The race for the prize: T-cell trafficking strategies for optimal surveillance

Blood ◽  
2012 ◽  
Vol 120 (7) ◽  
pp. 1432-1438 ◽  
Author(s):  
Minyi Lee ◽  
Judith N. Mandl ◽  
Ronald N. Germain ◽  
Andrew J. Yates
Keyword(s):  
T Cells ◽  
Lymph Node ◽  
T Cell ◽  
Optimization Problem ◽  
Cell Trafficking ◽  
T Cell Trafficking ◽  
Cell Responses ◽  
Major Histocompatibility Complexes ◽  
Draining Lymph Node ◽  
Slow Transit

Abstract The initiation of T-cell responses requires rare precursors to locate a draining lymph node (dLN) and encounter dendritic cells (DCs) presenting peptide-major histocompatibility complexes (pMHCs). To locate this needle in the haystack rapidly, T cells face an optimization problem—what is the most efficient trafficking strategy for surveillance and recirculation through blood? Two extremes are scanning low numbers of DCs per node with frequent recirculation, or meticulous surveillance with infrequent recirculation. Naive T cells also require stimulation by self-pMHCs. To enable efficient location of both foreign and self, has evolution settled on an optimum time for T cells to spend surveying each lymph node? Using a data-driven mathematical model, we show the most efficient strategy for detecting antigen in a dLN depends on its abundance. Detection of low-density antigen is optimized with systemically slow transit. In contrast, at high densities or if dLN egress is restricted, rapid transit through other nodes is optimal. We argue that blood-lymph recirculation dynamics facilitate a trade-off, and are consistent with dominant roles for the very early detection of rare foreign antigens in a dLN, and the efficient accumulation of signals from systemically distributed self-antigens.

scholarly journals Mechanisms of T cell-induced glomerular injury in anti-glomeruler basement membrane (GBM) glomerulonephritis in rats

1997 ◽  
Vol 109 (1) ◽  
pp. 134-142 ◽  
Author(s):  
X. R. HUANG ◽  
P. G. TIPPING ◽  
J. APOSTOLOPOULOS ◽  
C. OETTINGER ◽  
M. D'SOUZA ◽  
...  
Keyword(s):  
T Cell ◽  
Basement Membrane ◽  
Glomerular Injury

Gene Expression Profiling of Peripheral T-Cell Lymphoma (PTCL, NOS) and Comparison to Diffuse Large B-Cell Lymphoma (DLBCL).

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 2277-2277
Author(s):  
Daruka Mahadevan ◽  
Catherine Spier ◽  
Kimiko Della Croce ◽  
Susan Miller ◽  
Benjamin George ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lymph Node ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Gene Expression Profiling ◽  
Real Time ◽  
Expression Profiling ◽  
Cell Lymphoma ◽  
Rt Pcr

Abstract Background: WHO classifies NHL into B (~85%) and T (~15%) cell subtypes. Of the T-cell NHL, peripheral T-cell NHL (PTCL, NOS) comprises ~6–10% with an inferior response and survival to chemotherapy compared to DLBCL. Gene Expression Profiling (GEP) of DLBCL has provided molecular signatures that define 3 subclasses with distinct survival rates. The current study analyzed transcript profiling in PTCL (NOS) and compared and contrasted it to GEP of DLBCL. Methods : Snap frozen samples of 5 patients with PTCL (NOS) and 4 patients with DLBCL were analyzed utilizing the HG-U133A 2.0 Affymetrix array (~18,400 transcripts, 22,000 probe sets) after isolating and purifying total RNA (Qiagen, RNAeasy). The control RNA samples were isolated from normal peripheral blood (PB) B-cell (AllCell, CA), normal PB T-cell (AllCell, CA) and normal lymph node (LN). Immunohisto-chemistry (IHC) confirmed tumor lineage and quantitative real time RT-PCR was performed on selected genes to validate the microarray study. The GEP data were processed and analyzed utilizing Affymetrix MAS 5.0 and GeneSpring 5.0 software. Our data were analyzed in the light of the published GEP of DLBCL (lymphochip and affymtrix) and the validated 10 prognostic genes (by IHC and real time RT-PCR). Results : Data are represented as “robust” increases or decreases of relative gene expression common to all 5 PTCL or 4 DLBCL patients respectively. The table shows the 5 most over-expressed genes in PTCL or DLBCL compared to normal T-cell (NT), B-cell (NB) and lymph node (LN). PTCL vs NT PTCL vs LN DLVCL vs NB DLBCL vs LN COL1A1 CHI3L1 CCL18 CCL18 CCL18 CCL18 VNN1 IGJ CXCL13 CCL5 UBD VNN1 IGFBP7 SH2D1A LYZ CD52 RARRES1 NKG7 CCL5 MAP4K1 Of the top 20 increases, 3 genes were common to PTCL and DLBCL when compared to normal T and B cells, while 11 were common when compared to normal LN. Comparison of genes common to normal B-cell and LN Vs DLBCL or PTCL and normal T-cell and LN Vs PTCL or DLBCL identified sets of genes that are commonly and differentially expressed in PTCL and/or DLBCL. The 4 DLBCL patients analyzed express 3 of 10 prognostic genes compared to normal B-cells and 7 of 10 prognostic genes compared to normal LN and fall into the non-germinal center subtype. Quantitative real time RT-PCR on 10 functionally distinct common over-expressed genes in the 5 PTCL (NOS) patients (Lumican, CCL18, CD14, CD54, CD106, CD163, α-PDGFR, HCK, ABCA1 and Tumor endothelial marker 6) validated the microarray data. Conclusions: GEP of PTCL (NOS) and DLBCL in combination with quantitative real time RT-PCR and IHC have identified a ‘molecular signature’ for PTCL and DLBCL based on a comparison to normal (B-cell, T-cell and LN) tissue. The categorization of the GEP based on the six hallmarks of cancer identifies a ‘tumor profile signature’ for PTCL and DLBCL and a number of novel targets for therapeutic intervention.

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