Type II Collagen-Specific B Cells Induce Immune Tolerance in Th1-Skewed, Th2-Skewed, and Arthritis-Prone Strains of Mice

被引:5
作者
Farooq, Shukkur M. [1 ]
Ashour, Hossam M. [2 ,3 ]
机构
[1] Wayne State Univ, Dept Pharm Practice, Eugene Applebaum Coll Pharm & Hlth Sci, Detroit, MI 48201 USA
[2] Univ S Florida, Coll Arts & Sci, Dept Integrat Biol, St Petersburg, FL 33701 USA
[3] Cairo Univ, Dept Microbiol & Immunol, Fac Pharm, Cairo 11562, Egypt
关键词
ACAID; peripheral tolerance; immune privilege; regulatory T cells; collagen type II; B cells;
D O I
10.3390/cells10040870
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Antigen-specific regulatory T cells play key immune suppressive roles in autoimmune disease models and regulate the peripheral tolerance achieved via anterior chamber-associated immune deviation (ACAID). Articular cartilage has type II collagen (CII), which is a potent autoantigen protein in arthritis. There has not been much research on the clinical importance of CII-associated diseases. Moreover, the capability of CII to induce immune tolerance has not been previously assessed. We reported that delivery of CII either directly into the eye or via intravenous injection of CII-specific ACAID antigen presenting cells (APCs) can induce ACAID. Here, we hypothesized that peripheral tolerance can be induced following adoptive transfer of in vitro generated CII-specific ACAID B cells to naive mice. Delayed hypersensitivity (DTH) assays were used to assess the suppressive ability of adoptively transferred B cells. Immune responses of ACAID B cell-injected mice were significantly suppressed following challenges with CII as compared to positive controls. This effect was replicated in three different strains of mice (C57BL/6, BALB/c, and DBA/1). Thus, CII-specific ACAID B cells were able to induce immune tolerance in Th1-skewed, Th2-skewed, and arthritis-prone mice. ACAID B cell-mediated tolerance induced by CII could have therapeutic implications for the treatment of CII-mediated autoimmune diseases.
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页数:7
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共 36 条
  • [1] Expansion of B cells is necessary for the induction of T-Cell tolerance elicited through the anterior chamber of the eye
    Ashour, Hossam M.
    Niederkorn, Jerry Y.
    [J]. INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY, 2007, 144 (04) : 343 - 346
  • [2] Peripheral tolerance via the anterior chamber of the eye: Role of B cells in MHC class I and II antigen presentation
    Ashour, Hossam M.
    Niederkorn, Jerry Y.
    [J]. JOURNAL OF IMMUNOLOGY, 2006, 176 (10) : 5950 - 5957
  • [3] Hair follicle immune privilege and its collapse in alopecia areata
    Bertolini, Marta
    McElwee, Kevin
    Gilhar, Amos
    Bulfone-Paus, Silvia
    Paus, Ralf
    [J]. EXPERIMENTAL DERMATOLOGY, 2020, 29 (08) : 703 - 725
  • [4] Regulating the immune system: the induction of regulatory T cells in the periphery
    Buckner, JH
    Ziegler, SF
    [J]. ARTHRITIS RESEARCH & THERAPY, 2004, 6 (05) : 215 - 222
  • [5] Type II collagen autoimmunity in a mouse model of human rheumatoid arthritis
    Cho, Young-Gyu
    Cho, Mi-La
    Min, So-Youn
    Kim, Ho-Youn
    [J]. AUTOIMMUNITY REVIEWS, 2007, 7 (01) : 65 - 70
  • [6] D'Orazio TJ, 1998, IMMUNOLOGY, V95, P47
  • [7] Ocular immune privilege promoted by the presentation of peptide on tolerogenic B cells in the spleen. II. Evidence for presentation by Qa-1
    D'Orazio, TJ
    Mayhew, E
    Niederkorn, JY
    [J]. JOURNAL OF IMMUNOLOGY, 2001, 166 (01) : 26 - 32
  • [8] The in vivo and in vitro induction of anterior chamber associated immune deviation to myelin antigens in C57BL/6 mice
    Farooq, Shukkur M.
    Elkhatib, Walid F.
    Ashour, Hossam M.
    [J]. BRAIN BEHAVIOR AND IMMUNITY, 2014, 42 : 118 - 122
  • [9] In vitro-induced cell-mediated immune deviation to encephalitogenic antigens
    Farooq, Shukkur M.
    Ashour, Hossam M.
    [J]. BRAIN BEHAVIOR AND IMMUNITY, 2014, 35 : 64 - 69
  • [10] Eye-Mediated Induction of Specific Immune Tolerance to Encephalitogenic Antigens
    Farooq, Shukkur M.
    Ashour, Hossam M.
    [J]. CNS NEUROSCIENCE & THERAPEUTICS, 2013, 19 (07) : 503 - 510