CONTACTS
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Phone: (706) 721-3528
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Email: rpacholczyk@mail.mcg.edu
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Room: CA-4135
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Address:
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| Medical College of Georgia, |
| CBGM, 1120 15th Street, |
| CA4135, |
| Augusta, GA 30912 |
| MCG Faculty Page |
EDUCATION
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| Ph.D. degree in Biological Science in Immunology |
| Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Science, Wroclaw, Poland |
| M.S. in Biotechnology |
| Department of Fundamental Problems of Technology, University of Technology, Wrocław, Poland |
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RAFAL PACHOLCZYK:
ASSISTANT PROFESSOR
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Autoimmunity
Though the main strength of adaptive immunity is the diversity of T cell receptor (TCR) repertoire generated during its development in the thymus, it is also its weakness. This high diversity of TCR’s ensures the ability of the immune system to respond to different pathogens, but it also generates potentially autoreactive T cells that are exposed to tissue specific (extrathymic) self-antigens and continuously exposed to non-pathogenic antigens. The basis of immune tolerance is associated with the ability of the immune system to purge autoreactive T cells in the thymus and impose unresponsiveness in the periphery. This peripheral tolerance is implemented by T cell anergy, deletion or active suppression (regulatory T cells). Failure in the effectiveness of these processes leads to the development of many autoimmune diseases.
Our general research interest focuses on exploring mechanisms of autoimmunity and immune tolerance using in vivo and in vitro assays in mouse experimental models. We are trying to decipher how loss of tolerance and expansion of self-reactive lymphocytes lead to tissue damage with emphasis on T cell immunology.
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Immunopathogenesis of Sjogren’s Syndrome
Sjögren’s syndrome (SjS) is an autoimmune, chronic inflammatory disease affecting every population and racial group, and is the second most common connective tissue disease overall. The pathogenesis of autoimmune diseases is complex. Onset of clinical symptoms and eventual glandular dysfunction are highly dependent on autoantibodies produced by B cells. However, the central role in an onset of the pathogenesis of SjS is played by T cell-mediated autoimmunity. Unfortunately, there is little known about autoreactive T cells and the role of regulatory T (Treg) cells in the progression of SjS, especially that regulatory T cells play a pivotal role in controlling peripheral autoimmunity.
The overall goal of this project is to understand the sequential contribution of different autoreactive TCRs during glandular infiltration, the role of equilibrium between effector and regulatory CD4+ T cells bearing autoreactive TCRs and how it changes over time, and the function of subset of CD4 effector T cells in providing help to B cells within ectopic germinal centers.
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Effect of hyperglycemia on effector and regulatory CD4 T cells in NOD mice
Type 1 diabetes (T1D) is a direct consequence of a failure in immune tolerance to islet autoantigens in both humans and nonobese diabetic (NOD) mice. It is characterized by hyperglycemia and vascular complications arising from suboptimal control of blood level. It has been shown that acute hyperglycemia can initially induce an immunosuppression followed by homeostatic proliferation of T cells and that in chronic hyperglycemia initiation of adaptive immunity is impaired. Unfortunately a link between hyperglycemia and suppressed (induced) adaptive responses has received little attention.
The overall goal of this project is to understand the effect of hyperglycemia on diversity and specificities of different subsets of CD4 T cells during recovery phase, as well as during response to allogeneic islet transplantation
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Tie2cre-induced inactivation of the miRNA-processing enzyme Dicer disrupts invariant NKT cell development.
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Zhou L, Seo KH, He HZ, Pacholczyk R, Meng DM, Li CG, Xu J, She JX, Dong Z, Mi QS.
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Henry Ford Immunology Program, and Department of Dermatology, Henry Ford Hospital, Detroit, MI 48202, USA.
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