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- Autoimmunity (2)
- Myocarditis (2)
- Acanthamoeba castellanii (1)
- Acanthamoeba granulomatous encephalitis (1)
- Aconitase (1)
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- Autoreactive T cells (1)
- Cardiac myosin (1)
- Cardiac myosin heavy chain-α (1)
- Coxsackievirus B3 (1)
- Experimental autoimmune encephalomyelitis (1)
- Immune invasion (1)
- MHC class II dextramers (1)
- MHC class II tetramers (1)
- Molecular mimicry (1)
- Mouse model (1)
- Multiple sclerosis (1)
- Nitric oxide (1)
- Proteolipid protein (1)
- RAW 264.7 cells (1)
- Staphylococcus aureus (1)
Articles 1 - 5 of 5
Full-Text Articles in Life Sciences
Coxsackievirus B3 Infection Leads To The Generation Of Cardiac Myosin Heavy Chain-Α-Reactive Cd4 T Cells In A/J Mice, Arunakumar Gangaplara, Chandirasegaran Massilamany, Deborah M. Brown, Gustavo A. Delhon, Asit K. Pattnaik, Nora Chapman, Noel Rose, David J. Steffen, Jay Reddy
Coxsackievirus B3 Infection Leads To The Generation Of Cardiac Myosin Heavy Chain-Α-Reactive Cd4 T Cells In A/J Mice, Arunakumar Gangaplara, Chandirasegaran Massilamany, Deborah M. Brown, Gustavo A. Delhon, Asit K. Pattnaik, Nora Chapman, Noel Rose, David J. Steffen, Jay Reddy
Jay Reddy Publications
Enteroviruses like coxsackievirus B3 (CVB3) are common suspects in myocarditis/dilated cardiomyopathy patients. Autoimmunity has been proposed as an underlying mechanism, but direct evidence of its role is lacking. To delineate autoimmune response in CVB3 myocarditis, we used IAk dextramers for cardiac myosin heavy chain (Myhc)-α 334–352. We have demonstrated that myocarditis-susceptible A/J mice infected with CVB3 generate Myhc-α-reactive CD4 T cells and such a repertoire was absent in naïve mice as measured by proliferative response to Myhc-α 334–352 and IAk dextramer staining. We also detected Myhc-α 334–352 dextramer+ cells in the hearts of CVB3-infected mice. The autoreactive …
Tca Cycle Inactivation In Staphylococcus Aureus Alters Nitric Oxide Production In Raw 264.7 Cells, Chandirasegaran Massilamany, Arunakumar Gangaplara, Donald J. Gardner, James M. Musser, David J. Steffen, Greg A. Somerville, Jay Reddy
Tca Cycle Inactivation In Staphylococcus Aureus Alters Nitric Oxide Production In Raw 264.7 Cells, Chandirasegaran Massilamany, Arunakumar Gangaplara, Donald J. Gardner, James M. Musser, David J. Steffen, Greg A. Somerville, Jay Reddy
Jay Reddy Publications
Inactivation of the Staphylococcus aureus tricarboxylic acid (TCA) cycle delays the resolution of cutaneous ulcers in a mouse soft tissue infection model. In this study, it was observed that cutaneous lesions in mice infected with wild-type or isogenic aconitase mutant S. aureus strains contained comparable inflammatory infiltrates, suggesting the delayed resolution was independent of the recruitment of immune cells. These observations led us to hypothesize that staphylococcal metabolism can modulate the host immune response. Using an in vitro model system involving RAW 264.7 cells, the authors observed that cells cultured with S. aureus aconitase mutant strains produced significantly lower amounts …
Detection Of Cardiac Myosin Heavy Chain-Α-Specific Cd4 Cells By Using Mhc Class Ii/IaK Tetramers In A/J Mice, Chandirasegara Massilamany, Arunakumar Gangaplara, Nora M. Chapman, Noel Rose, Jay Reddy
Detection Of Cardiac Myosin Heavy Chain-Α-Specific Cd4 Cells By Using Mhc Class Ii/IaK Tetramers In A/J Mice, Chandirasegara Massilamany, Arunakumar Gangaplara, Nora M. Chapman, Noel Rose, Jay Reddy
Jay Reddy Publications
A/J mice bearing the H-2 allele IAk are highly susceptible to autoimmune myocarditis induced with cardiac myosin heavy chain (Myhc)-α 334–352, whereas B10.A mice carrying a similar allele IAk are relatively resistant, suggesting that the generation of Myhc-α-reactive T cell repertoires is influenced by genetic background. To enumerate the precursor frequencies of Myhc-α-specific CD4 T cells, we sought to create IAk tetramers for Myhc-α 334–352. Tetramers were created using approaches that involve covalent tethering of individual peptide sequences or exogenous loading of peptides into empty IAk molecules by peptide-exchange reaction. Using ribonuclease 43– 56 tetramers as controls, we demonstrated that …
An Epitope From Acanthamoeba Castellanii That Cross-React With Proteolipid Protein 139-151-Reactive T Cells Induces Autoimmune Encephalomyelitis In Sjl Mice, Chandirasegaran Massilamany, David Steffan, Jay Reddy
An Epitope From Acanthamoeba Castellanii That Cross-React With Proteolipid Protein 139-151-Reactive T Cells Induces Autoimmune Encephalomyelitis In Sjl Mice, Chandirasegaran Massilamany, David Steffan, Jay Reddy
Jay Reddy Publications
We report here that an epitope (aa, 83-95) derived from Acanthamoeba castellanii (ACA) induces clinical signs of experimental autoimmune encephalomyelitis (EAE) in SJL/J mice reminiscent of the disease induced with myelin proteolipid protein (PLP) 139-151. By using IAs/tetramers, we demonstrate that both ACA 83-95 and PLP 139-151 generate antigen-specific cross-reactive CD4 T cells and the T cells secrete identical patterns of cytokines and induce EAE with a similar severity. These results may provide insights into the pathogenesis of multiple sclerosis and ACA-induced granulomatous encephalitis.
Cutting Edge: Cd4+Cd25+ Regulatory T Cells Contribute To Gender Differences In Susceptibility To Experimental Autoimmune Encephalomyelitis, Jay Reddy, Hanspeter Waldner, Xingmin Zhang, Zsolt Illes, Kai W. Wucherpfennig, Raymond A. Sobel, Vijay K. Kuchroo
Cutting Edge: Cd4+Cd25+ Regulatory T Cells Contribute To Gender Differences In Susceptibility To Experimental Autoimmune Encephalomyelitis, Jay Reddy, Hanspeter Waldner, Xingmin Zhang, Zsolt Illes, Kai W. Wucherpfennig, Raymond A. Sobel, Vijay K. Kuchroo
Jay Reddy Publications
Female B10.S mice are highly resistant to proteolipid protein (PLP) 139–151-induced experimental autoimmune encephalomyelitis (EAE) and depletion of PLP 139–151- reactive CD4+CD25+regulatory T (Treg) cells can slightly increase their EAE susceptibility. Although male B10.S mice are moderately susceptible to EAE, we report that depletion of Treg cells in male B10.S mice before immunization with PLP 139–151 renders them highly susceptible to severe EAE with more CNS neutrophil infiltrates than nondepleted controls. Increased susceptibility is associated with an enhanced PLP 139–151-specific T cell response and greater production of IFN-γ, IL-6, and IL-17. Male CD4+CD25+ effector cells depleted of Treg cells proliferate …