scholarly journals Non-Major Histocompatibility Complex Control of Antibody Isotype and Th1 versus Th2 Cytokines during Experimental Infection of Mice with Mycobacterium avium

2001 ◽  
Vol 69 (3) ◽  
pp. 1708-1713 ◽  
Author(s):  
Vijaya Nagabhushanam ◽  
Christina Cheers
Keyword(s):  
Major Histocompatibility Complex ◽  
Antibody Response ◽  
Mycobacterium Avium ◽  
Enzyme Linked Immunosorbent Assay ◽  
Similar Response ◽  
Th2 Cytokines ◽  
Major Histocompatibility ◽  
Major Histocompatibility Complex Haplotype ◽  
Histocompatibility Complex ◽  
Ifn Γ

ABSTRACT Infection of different strains of mice withMycobacterium avium has revealed genetic control of the immunoglobulin isotype induced and of the balance between Th1 and Th2 cytokines. Female BALB/c or C57BL/10 mice were infected intranasally with 105 M. avium organisms. The antibody response was measured over 18 weeks by enzyme-linked immunosorbent assay and Western blotting, while numbers of cytokine-producing cells were assessed at 12 to 15 weeks by ELISPOT assay. Upon infection, C57BL/10 mice produced a clear Th1 response with strong gamma interferon (IFN-γ) production, no interleukin-4 (IL-4), and almost entirely immunoglobulin G2a (IgG2a) antibody. In contrast, BALB/c mice developed T cells producing IL-4, as well as those producing IFN-γ, while the antibody response was a mixture of IgG1 and IgG2a. Antibodies from BALB/c mice were also able to recognize a greater range of antigens than were C56BL/10 mice. B10D2 mice, which carry the BALB/c major histocompatibility complex haplotype on a C57BL/10 background, followed the C57BL/10 cytokine pattern. Mice infected withListeria monocytogenes did not show a similar response dichotomy.

scholarly journals Major histocompatibility complex recombinant R13 antibody response against bovine red blood cells

2020 ◽  
Vol 99 (10) ◽  
pp. 4804-4808
Author(s):  
N.G. Wilkinson ◽  
R.T. Kopulos ◽  
L.M. Yates ◽  
W.E. Briles ◽  
R.L. Taylor
Keyword(s):  
Major Histocompatibility Complex ◽  
Antibody Response ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Major Histocompatibility ◽  
Histocompatibility Complex

scholarly journals Major Histocompatibility Complex Haplotype Determines hsp70-Dependent Protection against Measles Virus Neurovirulence

2009 ◽  
Vol 83 (11) ◽  
pp. 5544-5555 ◽  
Author(s):  
Thomas Carsillo ◽  
Mary Carsillo ◽  
Zachary Traylor ◽  
Päivi Rajala-Schultz ◽  
Phillip Popovich ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Measles Virus ◽  
Protective Role ◽  
Major Histocompatibility ◽  
Major Histocompatibility Complex Haplotype ◽  
Brain Infection ◽  
Histocompatibility Complex ◽  
The Impact

ABSTRACT In vitro studies show that hsp70 promotes gene expression for multiple viral families, although there are few reports on the in vivo significance of virus-hsp70 interaction. Previously we showed that hsp70-dependent stimulation of Edmonston measles virus (Ed MeV) transcription caused an increased cytopathic effect and mortality in transgenic hsp70-overexpressing C57BL/6 mice (H-2 b ). The response to MeV infection is influenced by the major histocompatibility complex haplotype; H-2 d mice are resistant to brain infection due to robust antiviral immune responses, whereas H-2 b mice are susceptible due to deficiencies in this response. We therefore tested the hypothesis that the outcome of MeV-hsp70 interaction may be dependent upon the host H-2 haplotype. The impact of selective neuronal hsp70 overexpression on Ed MeV brain infection was tested with congenic C57BL/10 H-2 d neonatal mice. In this context, hsp70 overexpression conferred complete protection against virus-induced mortality, compared to >30% mortality in nontransgenic mice. Selective depletion of T-cell populations showed that transgenic mice exhibit a diminished reliance on T cells for protection. Brain transcript analysis indicated enhanced innate immune activation and signaling through Toll-like receptors 2 and 4 at early times postinfection for transgenic infected mice relative to those for nontransgenic infected mice. Collectively, results suggest that hsp70 can enhance innate antiviral immunity through Toll-like receptor signaling, supporting a protective role for physiological responses that enhance tissue levels of hsp70 (e.g., fever), and that the H-2 haplotype determines the effectiveness of this response.

scholarly journals Turkey humoral and cell-mediated immune responses to a Newcastle viscerotropic vaccine and its association with major histocompatibility complex.

2019 ◽  
Vol 22 (1) ◽  
pp. 26-40
Author(s):  
H. Al-Karagoly ◽  
G. Nikbakht ◽  
M. Hassanzadeh ◽  
T. Tolouei
Keyword(s):  
Major Histocompatibility Complex ◽  
Immune Responses ◽  
Mhc Class Ii ◽  
Cellular Response ◽  
Class Ii ◽  
Secretory Iga ◽  
Enzyme Linked Immunosorbent Assay ◽  
Major Histocompatibility ◽  
Exon 2 ◽  
Histocompatibility Complex

Immune responses to vaccines are mainly influenced by the nature of vaccines and host variation in response to vaccination. In this study we aimed to investigate turkey humoral and cell-mediated immune responses to a Newcastle viscerotropic vaccine and its association with major histocompatibility complex (MHC). Turkeys were vaccinated with Villegas–Glisson/University of Georgia (VG/GA) attenuated vaccine against Newcastle disease. The stimulation index of lymphocyte proliferation and antigen-specific local secretory IgA responses in bile, duodenum, ileum, as well as serum IgY and IgA responses were analysed by enzyme-linked immunosorbent assay. The turkey MHC class II B locus was selected as candidate gene for detection of associations with cellular and humoral immune responses. Significant differences were observed between both cellular and humoral responses of vaccinated and unvaccinated groups. A significant positive correlation was also found between ND specific IgY and ND specific IgA titres in serum, intestine (duodenum and ileum) and trachea. Moreover, the correlation between specific IgA titres in ileum and specific bile, duodenum and trachea was positively significant. High resolution melting analysis (HRM) was used to genotype MHC class II B exon 2. Eight melting profiles (A-G) were identified, among which, profile G showed a significant association with cellular response. The profile B revealed significant association with total IgA titres in serum and ileum. These findings help our understanding of the association of turkey MHC types with immune responses. Further correlation analysis between serum and mucosal antibody titres demonstrated that the levels of IgY and IgA in serum can give an impression about the levels of secretory IgA and situation of mucosal immunity. Based on the significant effects, ND specific IgY in serum appears to be a promising indirect marker for specific IgA in serum and trachea.

Abstract P097: Soluble TNF Receptor II Levels are Associated With Leukocyte DNA Methylation in the Major Histocompatibility Complex Region in the Framingham Heart Study

Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Michael M Mendelson ◽  
Roby Joehanes ◽  
Chunyu Liu ◽  
Tianxiao Huan ◽  
Chen Yao ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Major Histocompatibility Complex ◽  
Biological Process ◽  
Community Dwelling ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Receptor ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Protein Class ◽  
Soluble Tnf Receptor

Background: Transmembrane TNF receptors are involved in signal transduction for inflammatory, apoptotic, and proliferative processes, and can be shed into the bloodstream in response to various stimuli. Soluble TNF receptor II (sTNFR2) levels are predictive of incident cardiovascular disease events. We speculate that sTNFR2 is associated with ‘epigenetic priming’ of leukocytes in community dwelling adults, which may relate to the pathophysiology underlying atherogenic risk. Methods: We conducted a methylome-wide association study of sTNFR2 levels among participants in the Framingham Offspring cohort (examination 8; 2005-2008). Methylation of whole-blood derived DNA was assayed by microarray (Infinium HumanMethylation450 BeadChip, Illumina). sTNFR2 was quantitated by an enzyme-linked immunosorbent assay (Quantikine, R&D Systems). We excluded individuals with known autoimmune diseases or on medications that affect inflammatory response. We conducted linear mixed effects models adjusting for age, sex, body mass index, smoking, imputed cell count, and technical covariates. A Bonferroni-adjusted p-value for 485k tests (p<1x10 -7 ) was considered significant. sTNFR2-related CpGs were tested for enrichment in DNAse I Hypersensitivity (DHS) hotspots and overlapping chromatin marks across various cell and tissues lines from ENCODE, Epigenomics Roadmap and Blueprint data. Genes annotated to sTNFR2-related CpGs were tested for overrepresentation for protein class and biological process gene ontologies. Results: Our study included 2472 participants (mean±SD: age 66±9 years, 54% female, sTNFRII 2658±1093 pg/ml). In the multivariable-adjusted model, methylation at 168 CpGs was associated with sTNFR2 levels (p<10 -7 , λ GC =1.4). Identified CpGs were enriched in active regulatory regions (DHS hotspots) across most blood cell lines (especially inflammatory macrophages, p<10 -15 ), but also vascular and cardiac tissues (p<10 -4 ). sTNFR2-related CpGs were enriched in loci that overlapped histone modifications indicative of enhancers (H3K4me1), and to a lesser extent, promoters (H3K4me3) and actively transcribed gene bodies (H3K36me3). A substantial proportion of the identified CpGs (27 CpGs; 16%) were located in the major histocompatibility complex (MHC) region. Overall, there was enrichment in the protein class ‘MHC antigen’ (p=3x10 -5 ) and the biological process ‘antigen processing and presentation’ (p=2x10 -4 ). Other top loci were in gene regions involved in NF-κB/cytokine pathways, such as NLRC5 , SOCS3 , BCL3, and SBNO2 . Conclusions: We identify numerous loci in the MHC region and near specific NF-κB pathway genes that are differentially methylated in blood in relation to sTNFR2 levels. We present a foundation of candidate loci for future studies to determine relevance for targeting to prevent, treat, or improve risk prediction for cardiovascular disease.

scholarly journals Immune response genes controlling responsiveness to major transplantation antigens. Specific major histocompatibility complex-linked defect for antibody responses to class I alloantigens.

1982 ◽  
Vol 155 (1) ◽  
pp. 303-320 ◽  
Author(s):  
G W Butcher ◽  
J R Corvalán ◽  
D R Licence ◽  
J C Howard
Keyword(s):  
Major Histocompatibility Complex ◽  
Antibody Response ◽  
Antibody Responses ◽  
Class I ◽  
Control Analysis ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Transplantation Antigens ◽  
Ir Genes

We have identified two major histocompatibility complex (MHC)-linked Ir genes that control the antibody response made by rats against class I major alloantigens. We have named these genes Ir-RT1Aa and Ir-RT1Ac. These Ir genes determine responsiveness of the immunized animal in a typical codominant fashion. There is no evidence so far for trans-complementation between low-responder haplotypes. Detailed studies of Ir-RT1Aa indicate that it controls the antibody response to at least two distinct alloantigenic determinants on RT1Aa molecules. These class I molecules thus behave like hapten-carrier conjugates when the response against the carrier is under Ir gene control. Analysis of the origin of alloantibody-forming cells in tetraparental radiation chimeras indicates that Ir-RT1Aa must control the provision of effective help to B cells. In many respects therefore, the properties of Ir-RT1Aa are broadly similar to those described for Ir genes controlling antibody responses to conventional antigens. The existence of apparently conventional Ir genes controlling the antibody response to major alloantigens strongly suggest that the processing of these transmembrane molecules by host antigen-presenting cells is a prerequisite for immune induction, and that it is the MHC of the responder rather than that of the allograft to which T helper cells are restricted in alloimmune responses in vivo.

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