Monoclonal antibodies against antigens on human monocytes.
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Biomedical subjects
Publications and source records attributed to G R Russ.
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RM2.184, a mouse IgG2a monoclonal antibody, recognizes a polymorphic determinant on the complement receptor for C3bi which is present on granulocytes and monocytes. The RM2.184 epitope is distinct from the monomorphic determinant recognized by the monoclonal antibody OKM1. The RM2.184 epitope is probably on the alpha subunit and dependent on the association of the alpha and beta subunits for its configuration, as it can not be detected after the subunits have been dissociated. The phenotypic frequency of the RM2.184 antigen is approximately 14%, and its segregation in families is independent of HLA and consistent with an autosomal co-dominant mode of inheritance.
Twenty-four patients with severe hypertension (diastolic blood pressure (DBP) greater than 14.7 kPa (110 mmHg] were allocated at random to one of two treatment groups. All were given clonidine hydrochloride; twelve by intramuscular injection (Group 1), and 12 by intravenous injection (Group 2). The two routes were equally effective; diastolic blood pressure was reduced to less than 13.3 kPa (100 mmHg) in 11 patients in Group 1 and 10 patients in Group 2. The response in both groups was smooth, with no episodes of severe hypotension. Two patients in each group showed an initial transient pressor response. Clonidine hydrochloride, administered either intravenously or intramuscularly, is an effective treatment for severe hypertension but patients should be observed closely during the first hour after injection.
Patients with analgesic nephropathy are at risk from uro-epithelial malignancy. Enhanced secretion of beta 2-microglobulin occurs from epithelial cancer cells. In order to find a screening test for malignancy in analgesic nephropathy, urinary levels of this protein were measured in patients with analgesic nephropathy with urine cytological abnormalities and were compared to a control group with glomerulonephritis. Mean fractional excretion of beta 2-microglobulin was higher (8.61 +/- 1.76 SEM) in patients with analgesic nephropathy than in those with glomerulonephritis (1.13 +/- 0.76) (P less than 0.025). Those patients with analgesic nephropathy who had malignant cells in the urine had higher mean fractional excretion (18.56 +/- 5.77) than those with only atypical cells (8.5 +/- 2.0) (P less than 0.05) who in turn had higher mean values than those with normal cytology (2.12 +/- 0.62) (P less than 0.0025). It is suggested that the increased beta 2-microglobulin excretion in analgesic nephropathy is due to secretion from abnormal urothelial cells as well as reduced tubular catabolism. Beta 2-microglobulin may be of use as a screening test for malignancy in analgesic nephropathy.
Forty-eight women with urinary tract infection due to Co-trimoxazole sensitive organisms were randomly allocated to receive either two tablets (0.96 grams) of Co-trimoxazole twice a day for one day, four tablets (1.92 grams) of Co-trimoxazole as a single dose, or, two tablets of Co-trimoxazole twice a day for seven days. The infection cure rate was comparable in each group being 82%, 87% and 81% respectively. The patients who received the single dose had a high incidence of minor side effects. Accordingly one-day treatment appears to be the treatment mode of choice. Failure to respond to single dose or single day treatment may indicate those patients requiring investigation of their urinary tract.
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Human tonsil B cells include a subpopulation (30 per cent) of cells which lack LFA-1 antigen. Activation of tonsil B cells by culture with anti-IgM and interleukin-4 led to an increase in staining intensities and in the proportion of cells staining, until by 48 h the majority of B cells were positive. Culture of activated cells with low-molecular weight B cell growth factor, which induces a proportion of cells to proliferate, led to a minor further increase in expression of the LFA-1 antigen. Inclusion of a monoclonal antibody against the LFA-1 beta chain in culture did not affect either proliferation or immunoglobulin secretion. The expression of LFA-1 by B cells thus changes as B cells are activated, perhaps reflecting the changing requirements of B cells for interaction with other cells and tissue components. On the other hand, our results did not provide any support for the idea that the LFA-1 antigen is directly involved in the interaction of B cells with lymphokines which control proliferation and differentiation.