01934nas a2200217   4500000000100000008004100001260001300042653001200055653002300067653001700090653001100107653003000118653002300148653002300171100001800194245020900212300001100421490001500432520125500447022001401702       1992                            d  c1992 Oct10aAnimals10aAntibody Formation10aAutoimmunity10aHumans10aHypersensitivity, Delayed10aImmunity, Cellular10aParasitic Diseases1 aBretscher P A00aAn hypothesis to explain why cell-mediated immunity alone can contain infections by certain intracellular parasites and how immune class regulation of the response against such parasites can be subverted.  a343-510 v70 ( Pt 5)3 a<p>Cells with a low density of parasite-specific antigens on their surface are postulated to be susceptible to a cell-mediated attack but not to effector mechanisms normally activated following the binding of specific antibody to the infected cell. It is further postulated that such infected cells normally induce a cell-mediated response, and that cells infected with slow-growing intracellular parasites have a low density of parasite-specific antigens on their surface. Despite these general postulates, cell-mediated immunity is not invariably induced following natural infection by certain slow-growing parasites, such as those responsible for leprosy, tuberculosis, and the leishmaniases, and antibody can be induced that is exclusive of a strong, cell-mediated response. It is proposed that certain events in such cases subvert the normal regulatory processes that control the class of immunity induced. In these cases, the parasite-infected cells, bearing a low representation of parasite antigens, induce antibody even though they are not susceptible to antibody-dependent effector mechanisms, and so they are not eliminated. In this case, chronic infection and uncontrolled growth of the parasite occurs, often with fatal consequences.</p>  a0818-9641