       Document 0402
 DOCN  M9640402
 TI    T helper cell dichotomy to Candida albicans: implications for pathology,
       therapy, and vaccine design.
 DT    9604
 AU    Romani L; Cenci E; Menacci A; Bistoni F; Puccetti P; Department of
       Experimental Medicine and Biochemical Sciences,; University of Perugia,
       Italy.
 SO    Immunol Res. 1995;14(2):148-62. Unique Identifier : AIDSLINE
       MED/96108418
 AB    Acquired immunity to Candida albicans is believed to prevent mucosal
       colonization of adult immunocompetent individuals from progressing to
       symptomatic infection. Resistance to disease appears to correlate with
       the detection of delayed-type hypersensitivity responses in vivo and a T
       helper type 1 (Th1) cytokine secretion profile in vitro. Cellular
       immunodeficiency, particularly HIV infection, greatly increases the risk
       of mucosal infection, confirming that CD(4+)-cell-directed immunity is
       effective locally in controlling infectivity of the yeast. While
       Th1-type CD4+ cell activation resulting in phagocyte-dependent immunity
       clearly represents an important mechanism of anticandidal resistance,
       clinical observations suggest that Th2-type CD4+ cell reactivity may be
       triggered by Candida antigens in several disease states, including
       symptomatic infections and immunopathology. This may imply that a
       Th1-type pattern of reactivity characterizes the saprophytic yeast
       carriage and resistance to disease by healthy humans, whereas Th2-type
       responses would be mostly associated with pathology. Moreover,
       Candida-specific T helper responses, namely humoral and cell-mediated
       immunity, appear to be reciprocally regulated, as typically occurs in
       experimental models of parasitic and retroviral infection, where the
       Th1/Th2 paradigm of acquired immunity has been best characterized.
       Recent studies, besides providing direct evidence for the occurrence of
       cross-regulatory Th1 and Th2 responses in mice with candidiasis,
       emphasize the potential of cytokine/anticytokine therapy for recruiting
       Candida-specific responses toward protective, Th1-type CD4+ cell
       reactivity. At the same time, these studies call attention to the
       possible consequences of C. albicans infection for immunopathology,
       allergy, and coinfection.
 DE    Animal  Candida albicans/*IMMUNOLOGY  *Candidiasis/PATHOLOGY/PREVENTION
       & CONTROL/THERAPY  Drug Design  Fungal Vaccines/*THERAPEUTIC USE  Human
       Support, Non-U.S. Gov't  *T-Lymphocytes, Helper-Inducer  JOURNAL ARTICLE
       REVIEW  REVIEW, TUTORIAL

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

