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H K Muller

Publications and source records attributed to H K Muller.

134 records · Page 8Linked to original sources
PubMed1971

Immunofluorescent staining of rat gastric parietal cells by human antibody unrelated to pernicious anaemia.

Immunofluorescence tests on 94 human sera reacting with rat gastric parietal cells revealed that 41 (44%) of the sera contained antibody to a rat parietal cell antigen that was distinct from the pernicious anaemia autoantigen. Ten of the sera contained antibodies to both parietal cell antigens. The remaining 53 (56%) sera contained only parietal cell antibodies of the pernicious anaemia type. We recommend that mouse gastric mucosa, which does not react with the heterologous rat parietal cell antibody, replace rat gastric mucosa for immunofluorescence diagnostic tests.

Anemia, Pernicious↗
PubMedDate not supplied

Langerhans cell alterations in cutaneous carcinogenesis.

Analysis of the early stages of experimental skin cancer in mice has demonstrated that complete chemical carcinogens (e.g. DMBA or benzo(a)pyrene) and tumour promoters (e.g. TPA) but not tumour initiators (e.g. urethane) deplete or functionally alter epidermal Langerhans cells (LC). These changes result in altered local immunity as antigen presentation through LC depleted skin results in either immune tolerance due to the generation of suppressor T cells or anergy. Parallel studies in sheep have shown that, following the application of DMBA, depletion of LC is due to increased migration of these cells from the skin whereas tumour initiators did not alter LC migration. Likewise benzo(a)pyrene did not trigger enhanced LC migration from the epidermis. Experiments in mice suggest that part of this increased migration after the application of DMBA is due to the carcinogen being handled as an antigen by the epidermal LC. However, this fails to explain the prolonged migration which follows. The implication of these studies is that early in carcinogenesis, altered immune function occurs as a result of LC depletion/modification, allowing aberrant cells to proliferate in the absence of immune destruction.

Animals↗