PubMed Health⌕ Search

Biomedical subjects

C H Kirkpatrick

Publications and source records attributed to C H Kirkpatrick.

At least 37 records · Page 2Linked to original sources
PubMed1977

Autoimmune vitiligo: detection of antibodies to melanin-producing cells.

Vitiligo, a disorder characterized by the destruction of melanocytes, is often associated with diseases in which there are increased frequencies of autoantibodies. For this reason we investigated two patients with vitiligo, alopecia universalis, mucocutaneous candidiasis, and multiple endocrine insufficiencies for antibodies to melanin-producing cells. Using direct immunofluorescence of normal and vitiliginous skin from both patients and indirect immunofluorescence with both patients' serum, we could not detect these antibodies. However, an immunofluorescent complement-fixation test demonstrated a circulating antibody that bound to melanocytes in human skin, nevus cells and melanoma cells. Specificity of cellular fluorescence for nevus and melanoma cells was shown on serial sections stained with hematoxylin and eosin and was inferred for melanocytes from their distribution in human skin and their presence when the normal but not vitiliginous skin of both patients was used as substrate. This antibody was characterized as an IgG that activated complement via the classical pathway.

Adolescent↗
PubMed1977

Study of possible mechanisms of basophil accumulation in experimental cutaneous candidiasis in guinea pigs.

It is known that certain lymphokine preparations, bacterial growth products, and factors released through complement activation have in vitro chemotactic activity for basophils. We have developed a model for acute cutaneous candidiasis in guinea pigs in which the lesions are characterized by infecting organisms in the keratin layer, early accumulation of polymorphonuclear leukocytes in the upper epidermis, and subsequent accumulation of basophils along the dermal basement membrane. The present study was undertaken to determine if any of the known chemotactic factors were operating in vivo to attract basophils. Both nonimmune guinea pigs and animals with established delayed hypersensitivity to candida had basophils in the infected skin. While immune animals showed more basophils than did nonimmune animals, the difference was not significant. Intradermal injections of a sonicate of candida or a candida growth filtrate did not cause significant accumulation of basophils. Decomplementation of the animals with cobra venom factor (CVF) did not significantly reduce the basophil numbers. Moreover, basophil accumulation occurred in animals with only minimal serum antibody to candida. These studies indicate that the basophil accumulation is due to a mechanism that is not dependent on cellular immunity, direct chemotactic activity in the candida extract, antibodies, or complement. Therefore, there may exist a previously unrecognized, nonimmunologic mechanism of chemotaxis for basophils which could possibly operate in other types of lesions and could even be involved with attraction of other types of cells.

Animals↗
PubMed1977

Effects of levamisole on normal and abnormal leukocyte locomotion.

The anti-helminthic drug levamisole hydrochloride has been reported to stimulate immune responses in humans and experimental animals. We have investigated levamisole effects on human leukocyte locomotion in vitro in studies of neutrophils and mononuclear cells from normal adults, from patients with Chediak-Higashi disease and from patients with the syndrome of hyperimmunoglobulin E, recurrent pyogenic infections, and defective leukocyte chemotaxis. Directed migration (chemotaxis) of neutrophils and mononuclear cells from normal adults and from the hyperimmunoglobulin E syndrome patients, but not from Chediak-Higashi patients, were stimulated by levamisole at concentrations of 0.01-1.0 micronM, with stimulation observed most consistently at 0.1 micronM. These concentrations of drug also increased cyclic GMP levels in mononuclear cells and enhanced hexose monophosphate shunt activity in neutrophils, but did not alter chemotactic factor-induced changes in the surface charge of neutrophils. Other concentrations of levamisole did not affect leukocyte locomotion except for a high concentration (5.0 mM) which stimulated both random and directed leukocyte migration. When patients with the hyperimmunoglobulin E syndrome took levamisole by mouth, the abnormal chemotactic responses of their neutrophils were significantly improved towards normal. These studies are the first to show pharmacologic improvement of in vitro leukocyte locomotion in patients in whom recurrent infections have been attributed to a defect of this leukocyte function.

Adolescent↗
PubMed1976

Deposition of complement in the lesions of experimental cutaneous candidiasis in guinea pigs.

Deposits of C3 have been demonstrated at the dermo-epidermal junction in the lesions of experimental cutaneous candidiasis in guinea pigs. The deposits were granular in character and similar to those previously found in the lesions of chronic mucocutaneous candidiasis in humans. Immunoglobulin, C4 and candida antigen were not detected in the lesions. C3 was also found in a similar pattern at the dermo-epidermal junction of candida-infected skin from homozygous C4-deficient guinea pigs. From these observations, it is postulated that complement deposition occurs in these lesions as a result of alternative pathway activation, perhaps by cell wall components from the infecting organisms.

Animals↗
PubMed1976

Cellular immunity in Peyer's patches of rats infected with Trichinella spiralis.

A rat model of Trichinella spiralis gut infection was used to observe the sequence of developing cellular immunity in Peyer's patches and other lymphoid tissues. Whereas cellular reactivity (lymphocyte blastogenesis) for worm antigens was evident in mesenteric lymph nodes draining the gastrointestinal tract within 3 days after infection, Peyer's patch lymphocytes developed maximal reactivity 2 to 3 weeks later at the same time as the spleen and other lymphoid tissues. Furthermore, the immune reactivity found in Peyer's patches was only transient. Thus, in this parasitic gut infection, the Peyer's patch lymphoid tissue does not appear to be the first site of cellular responsiveness but rather to acquire cellular reactivity only when other lymphoid elements in the infected host have also acquired similar antigen-induced reactivity.

Animals↗
PubMed1976

Mechanisms involved in elimination of organisms from experimental cutaneous Candida albicans infections in guinea pigs.

Experimental cutaneous Candida albicans infections were produced in guinea pigs either by using occlusive dressings over the organisms or by applying them to the shaved skin directly without occlusive dressings. In either model there was clearance of the infecting organisms from the skin by a process involving profuse scaling of the keratinized layer in which they were confined. However, for each type of infection the mechanisms producing this scaling seemed to involve different parts of the host defense system. Infections produced under occlusive dressings were characterized by a rapid accumulation of polymorphonuclear leukocytes (PMN) in the epidermis and formation of thick crusts in which organisms were trapped. Sloughing of the crust removed the organisms. In this model, evolution of the lesions and the rate of clearance of the organisms did not depend on prior immunity to Candida. Two possible mechanisms for attraction of PMN into the lesions were direct activation of the alternative complement pathway by the organisms in the lesions and direct chemotactic activity in components of Candida albicans. In contrast, infections produced without occlusive dressings showed only minimal epidermal PMN infiltration, but also underwent profuse scaling of the keratinized layer. This response appeared to depend on cell-mediated immunity. Only animals with previously-acquired delayed hypersensitivity to Candida antigens could undergo this type of scaling, and indeed, this response was transferable to nonimmue animals with peritoneal exudate cells from Candida-immune animals. Clearance of the infecting organisms from this type of infection was significantly faster in immune than in nonimmune animals. It is postulated that a lymphokine released from lymphocytes in the upper epidermis acts on epidermal cells to increase the rate of keratin turnover either by the mitotic rate of the germinal cells or by increasing their rate of keratinization.

Animals↗
PubMed1976

Reconstitution of defective cellular immunity with foetal thymus and dialysable transfer factor. Long-term studies in a patient with chronic mucocutaneous candidiasis.

Extensive studies of a 9-year-old boy with recurrent pulmonary infections and chronic mucocutaneous candidiasis disclosed a severe defect in cell-mediated immunity but normal humoral immune responses. These immunological defects were not improved by initial treatment with transfer factor. After receiving a foetal thymus transplant the patient developed positive delayed-type skin tests, could be sensitized with chlorodinitrobenzene, and showed progressive improvement of in vitro lymphocyte functions including spontaneous formation of rosettes with sheep erythrocytes and positive responses to phytohaemagglutinin, concanavalin A and allogeneic leucocytes. Moreover, lymph node cellularity increased, especially in the thymus-dependent zones. Though the in vitro responses persisted for over 1 year, skin tests became unreactive at 38 weeks. However, in contrast to the pre-transplant experience transfer factor was now effective in inducing positive skin tests. These studies provide a chronological account of the effect of the thymus on expression of lymphocyte-mediated immune responses in man and suggest that thymus-derived cells are required for acquisition of transfer factor-induced cellular immunity.

Candidiasis, Cutaneous↗
PubMed1975

Selective hypogammaglobulinemia with persistence of IgE, malabsorption and a nutritionally dependent, reversible defect in cell-mediated immunity.

A 46 year old man presented with selective hypogammaglobulinemia, malabsorption and long-standing secondary malnutrition. Although the patient had essentially unmeasurable levels of immunoglobulins G (IgG), M (IgA), he had normal levels of immunoglobulin E (IgE). He was found to be anergic when tested for the delayed cutaneous hypersensitivity reaction. Evaluation of his cell-mediated immunity in vivo and in vitro suggested one discrete lesion, a defective production of the lymphocyte mediator macrophage migration inhibitory factor. With improved nutrition the patient "repaired" this defect in the "efferent" limb of cellular immunity and was no longer anergic.

Agammaglobulinemia↗