Lack of apoptosis of infiltrating cells as the mechanism of high susceptibility to EAE in DA rats

M. L. Lukic, E. Mensah-Brown, Sehamuddin Galadari, A. Shahin

    Research output: Contribution to journalArticle

    Abstract

    Dark Agouti (DA) rats are highly susceptible to induction of Th-1-mediated autoimmunity disease, including experimental allergic encephalomyelitis (EAE). In contrast to other susceptible rat strains in which disease is induced only with encephalitogen emulsified in complete Freund's adjuvants (CFA), in DA rats EAE develops after injection of encephalitogen in incomplete Freund's adjuvants (IFA) or Titermax, putative Th-2 directed adjuvant. Lymph node cells derived from immunized DA rats and stimulated in vitro produce significantly more Interferon-γ (IFN-γ) than resistant Albino Oxford (AO) rats. However, cells derived from both strains produce large amounts of IL-10 but not IL-4. Immunized lymph node cells derived from EAE susceptible (AO × DA) F1rats induce clinical signs of disease in sublethally irradiated parental DA but not AO rats. The pathohistology of the target tissue in these recipients clearly demonstrated infiltration of mononuclear cells in both parental strains. However, the number of CD4+ cells was significantly higher and number of apoptotic cells significantly lower in DA rats sacrificed 8 days after passive transfer. We postulate that in addition to higher IFN-γ and TNF-α production, resistance to early apoptosis of the invading cells in the target tissue possibly due to lack of downregulation by TGF-β leads to exceptional susceptibility to EAE in DA rats.

    Original languageEnglish (US)
    Pages (from-to)193-200
    Number of pages8
    JournalDevelopmental Immunology
    Volume8
    Issue number3-4
    StatePublished - Dec 1 2001

    Fingerprint

    Autoimmune Experimental Encephalomyelitis
    Apoptosis
    Interferons
    Cell Count
    Lymph Nodes
    Freund's Adjuvant
    Dasyproctidae
    Autoimmunity
    Interleukin-4
    Interleukin-10
    Down-Regulation
    Injections

    Keywords

    • Adjuvants
    • Apoptosis
    • Cytokines
    • EAE

    ASJC Scopus subject areas

    • Immunology
    • Developmental Biology

    Cite this

    Lukic, M. L., Mensah-Brown, E., Galadari, S., & Shahin, A. (2001). Lack of apoptosis of infiltrating cells as the mechanism of high susceptibility to EAE in DA rats. Developmental Immunology, 8(3-4), 193-200.

    Lack of apoptosis of infiltrating cells as the mechanism of high susceptibility to EAE in DA rats. / Lukic, M. L.; Mensah-Brown, E.; Galadari, Sehamuddin; Shahin, A.

    In: Developmental Immunology, Vol. 8, No. 3-4, 01.12.2001, p. 193-200.

    Research output: Contribution to journalArticle

    Lukic, ML, Mensah-Brown, E, Galadari, S & Shahin, A 2001, 'Lack of apoptosis of infiltrating cells as the mechanism of high susceptibility to EAE in DA rats', Developmental Immunology, vol. 8, no. 3-4, pp. 193-200.
    Lukic, M. L. ; Mensah-Brown, E. ; Galadari, Sehamuddin ; Shahin, A. / Lack of apoptosis of infiltrating cells as the mechanism of high susceptibility to EAE in DA rats. In: Developmental Immunology. 2001 ; Vol. 8, No. 3-4. pp. 193-200.
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