Murine transfer factor. II. Transfer of delayed hypersensitivity to synthetic antigens

Synthetic polyaminoacid antigens were used to examine the specificity of transfer of delayed-type hypersensitivity with spleen cell dialysates in mice. Dialysates from GAT10-sensitized donors sensitized recipients to GAT10, but not GLA5 or cytochrome c. Dialysates from GLA5-sensitized donors sensitized recipients to GLA5, but not GAT10 or cytochrome c. We interpret these findings as consistent with the concept that passive transfer of delayed hypersensitivity with dialyzable materials is an immunologically specific event.     

Transfer of delayed hypersensitivity to leishmanin (Montenegro reaction).

It was possible to transfer the cutaneous leishmanin hypersensitivity (Montenegro reaction) to 7 out of 12 recipients. The diameter of the indurations observed ranged from 8 to 25 mm. Histological examination of skin biopsies from the site of three positive Montenegro reactions showed intense mononuclear infiltrate of lymphocytes and histiocytes, and one biopsy showed the feature of tuberculoid granuloma. Four recipients retested with leishmanin after 11, 22, 25, and 32 days, still showed positive reactions.     

Modulation of delayed hypersensitivity in mice by cobra venom factor.

The effect of administration of purified cobra venom factor (CoF) on both induction and expression of delayed hypersensitivity (DH) to sheep red blood cells in mice was studied. Injection of CoF before immunization resulted in enhanced DH, whereas CoF treatment before elicitation suppressed the response. These effects could not directly be associated with reduced serum C₃ levels. CoF induced a stimulation of the mononuclear phagocytic system as measured by the clearance of colloidal carbon from the blood. A relation between this stimulatory effect and the modulation of DH is discussed. It is suggested that the macrophage is a major target cell of this CoF action.     

Transfer factor therapy in a case of complex immunodeficiency

A young woman with unclassified complex immune deficiency disease characterized by relapsing skin ulcerations, greatly depressed cellular immunity, absent serum IgA, and inability to develop circulating antibodies to typhoid vaccine, was treated twice with the dialyzable transfer factor from normal persons. Following such therapy she showed clinical improvement and strong delayed skin sensitivity to Candida, streptokinase-streptodornase, and moderate, rather short-lived hypersensitivity to PPD. In addition, she could be sensitized to dinitrochlorobenzene and her leucocytes responded normally to phytohaemagglutinin; all these manifestions of cellular immunity had been absent prior to therapy. She acquired the capacity to develop anti-typhoid antibodies.These findings appear to indicate that dialyzable transfer factor not only transfers delayed-type hypersensitivities preexisting in the donor but is also able to remedy hitherto unspecific defects existing in certain forms of immune deficiency.     

X-linked severe combined immunodeficiency: from molecular cause to gene therapy within seven years

X-linked severe combined immunodeficiency (XSCID) is the most common form of SCID. The discovery of the genetic defect in this disease, namely mutations in the gene encoding the common cytokine receptor gamma chain, gammac, was reported just over seven years ago. In the subsequent period, a tremendous amount of knowledge about the biology and function of this protein has been generated. Moreover, gammac-knockout mice have been generated and their immune systems successfully reconstituted by gene therapy. Furthermore, initial attempts at using gene therapy to treat patients with XSCID have been successful for more than ten months, making this disease perhaps the most promising to date for treatment with such a strategy.