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Biomedical subjects

M E Nichols

Publications and source records attributed to M E Nichols.

At least 37 records · Page 2Linked to original sources
PubMed1987

Monoclonal anti-K14 and anti-K2.

Mouse hybridoma clones have produced monoclonal antibodies directed against the K:14 and K:2 high-incidence antigens of the Kell blood group system. Two examples of anti-K14 were isolated, each arising from a separate fusion procedure. All three monoclonal antibodies are of the immunoglobulin class IgG1. Serological activity is consistent with that seen with human antibodies to high-incidence Kell system antigens, and their epitopes are destroyed, as usual, by 2-aminoethylisothiuronium bromide treatment. Specificity was further confirmed by adsorption and elution studies. Tests against nonhuman primate red cells demonstrated the expression of K:14 only by the great apes, whereas K:2 was present on all red cells tested. These findings emphasize the usefulness of monoclonal antibodies to elucidate the evolutionary patterns of blood group variants.

Animals↗
PubMed1987

Structural polymorphism of glycophorins demonstrated by immunoblotting techniques.

We have explored the polymorphism of the glycophorin system in the human erythrocyte membrane using the immunoblotting techniques and examining 52 individuals selected without prior bias as to their serologic state and ten documented serologic variants of M, N, S, s blood group system. Polyclonal antisera to alpha glycophorin and to alpha glycophorin CNBr carboxyl terminal fragment C (residues 82-131) and M and N specific monoclonal antibodies (MoAbs) were used. The first two reagents detect specific regions of the alpha glycophorin molecule and all electrophoretically resolved species of glycophorins immunologically related to alpha and delta glycophorins (delta glycophorin, [alpha-delta] hybrids and other glycophorins with an alteration in the carboxyl terminal segment); the M and N MoAbs identified the glycophorin species containing or lacking the M or N determinant in the amino terminal octapeptide structures. We find that immunoblotting confirmed in all cases the serologically determined phenotype; we also find that polymorphic forms of the glycophorin system are relatively infrequent; immunoblotting, independent from serologic testing, was capable of detecting five mutants, two most likely S-s-U-phenotypes; a new glycophorin species was detected in normal red cells with both antiglycophorin and antipeptide C sera, which is not evident with MoAbs; immunoblots of known glycophorin variants (En(a-), U-, Mg, Mi I, II, III, V, and Sta) confirmed but also extended our knowledge of the abnormal glycophorins involved; and the He+ and Wrb(-) cells showed normal patterns.

Glycophorins↗
PubMed1985

Two blood group M epitopes disclosed by monoclonal antibodies.

Two cloned mouse hybridomas, designated G8 and E3, produced anti-M of immunoglobulin classes IgG2b and IgG1, respectively. No discrepancies were observed in testing over 5,000 normal donor blood samples with appropriately diluted G8 and E3 culture supernatant fluids in parallel with rabbit anti-M and anti-N typing reagents. The specificity and titer of antibodies produced by G8 and E3 were minimally affected by changes in temperature (37 degrees C, 22 degrees C, 4 degrees C). G8 and E3 showed reduced activity with type MM red cells that had been treated with either neuraminidase or papain, but differences were observed in the susceptibility of the respective epitopes to treatment with neuraminidase. Furthermore, G8 and E3 exhibited different specificities when used to test the red cells of nonhuman primates and erythrocytes of the rare MgMg human blood type. These results indicate the existence of at least two M antigen epitopes.

Amino Acid Sequence↗
PubMed1985

Human erythroid progenitor cells express Rhesus antigens.

The expression of Rhesus antigens on hematopoietic progenitor cells was studied using monoclonal antibodies. Because these antibodies are not capable of lysing mature red blood cells in a complement-dependent cytotoxicity assay, fluorescence-activated cell sorting was performed. Using the monoclonal anti-Rh 29 antibody B10, 68% +/- 6% of the mature erythroid progenitor cells (CFU-E) were sorted into the positive fraction, while only 2% +/- 1% of the relatively immature erythroid progenitor cells (BFU-E), and 3% +/- 1% of the granulocyte-macrophage progenitor cells (CFU-GM) were cultured from this same fraction. Thus up to a 15-fold enrichment of CFU-E could be obtained. In two experiments more than 4% of the cells in the positive fraction consisted of CFU-E; in one experiment even more than 7% did. Using fractionated cell sorting, the Rhesus antigens appeared to have a lower density on CFU-E than HLA-DR determinants. Antibodies against the Rhesus antigens can be applied to enrich erythroid-committed stem cells and to separate mature from immature erythroid progenitor cells.

Antibodies, Monoclonal↗
PubMed1977

Anti-Lu14: a Lutheran antibody defining the product of an allele at the Lu8 blood group locus.

A 'new' Lutheran-related antibody, named anti-Lu14, reacts with approximately 2.4% of random bloods. Red cells of the rare Lu:-8 phenotype are Lu:14. The data indicate, with a high probability, that the Lu 14 antigen is a product of an allele of Lu8 and that Lu14 and Lu8 comprise a third pair of alleles at the Lutheran locus. Red cells of the original Sw (a+) propositus are Lu:14. By coincidence, he has inherited two low-incidence genes. This observation may explain the discrepancy in different families concerning a possible relationship between Swa and Lutheran. Pedigree information now suggests that Swa is not a Lutheran gene.

Alleles↗
PubMed1976

Kx antigen, the McLeod phenotype, and chronic granulomatous disease: further studies.

Leukocytes of nine unrelated boys with X-linked chronic granulomatous disease lack Kx antigen. In three of these cases, the red cells also lack Kx and have the McLeod phenotype and abnormal morphology. X-linked chronic granulomatous disease CGD can thus be separated into two types. Type I cases have an antigenic deficiency that is restricted to the phagocytic leukocytes while in type II, the deficiency involves both leukocytes and red cells. Red cells of type II CGD patients have enhanced i antigen activity suggesting that they are under hemopoietic stress. Normal Kx synthesis is directed by an X-linked gene named X1k. Three variants, X2k, X3k, and X4k order the different permutations of leukocyte and red cell Kx antigen production that have been recognized.

Blood Group Antigens↗
PubMed1976

In vivo and in vitro activation of T-antigen receptors on leukocytes and platelets.

Serological studies on a patient whose red cells are polyagglutinable due to T activation have demonstrated concomitant T activity of the separated leukocytes and platelets. Normal leukocytes and platelets are not T active, but activation can be induced in vitro by treatment with neuraminidase or with pneumococcus type III filtrate. Such T-active cells absorb anti-T from Arachis hypogea lectin. Tests on idfferent types of separated leukocytes show that both neutrophils and lymphocytes have latent T antigen receptors. Neuraminidase treatment of platelets does not change their ability to promote clot retraction, to aggregate with ADP, or to take up serotonin.

Absorption↗
PubMed1975

Chronic granulomatous disease and the Kell blood groups.

Fifteen antigenic determinants are known to be related to the Kell blood group. Some boys with X-linked chronic granulomatous disease have the very rare McLeod or Ko phenotype on their red cells. Serological studies of the McLeod type suggest that the weak Kell antigens that are present differ qualitatively and quantitatively from those on red cells of common Kell type. A new antigen, Kx, has been characterized and shown to be present on red cells and neutrophil leucocytes. Lack of red-cell Kx is associated with the McLeod phenotype, lack of leucocyte Kx is associated with chronic granulomatous disease.

Antigen-Antibody Reactions↗
PubMedDate not supplied

Inherited mosaicism affecting the ABO blood groups.

Blood samples from two families and three other unrelated people contain a mixture of red blood cells of two different ABO types. Previously described causes of red blood cell mosaicism have been excluded from responsibility. Other blood group systems are not involved. The phenotypes, which have been designated ABO mos, are inherited through a variant allele at the ABO locus and appear to arise from a change in regulation of an ABO gene of some somatic cells.

ABO Blood-Group System↗
PubMedDate not supplied

Naturally occurring anti-Kell stimulated by E. coli enterocolitis in a 20-day-old child.

Anti-A and anti-K have been found in the serum of a 20-day-old child who had not been transfused but who was acutely ill with E. coli enterocolitis. Both antibodies are IgM proteins. The mother's serum does not contain either antibody and the anti-A and anti-K in the infant's serum are not of maternal origin. Both parents and the child are of the Kell phenotype K-k+. Stool cultures made from the child yielded E. coli O 125:B15, an uncommon B-variant pathogenic coliform. Cell-free preparations made from broth cultures of this organism have strong specific inhibitory activity against IgM anti-A and anti-K, and both antigens have been identified on the bacterial cells. At age 3 months the child had made a clinical recovery, stool cultures showed no pathogenic coliforms, and anti-A and anti-K were no longer detectable in her serum. These data indicate that absorption of metabolites with A-like and K-like activity produced by a pathogenic coliform in the intestinal tract were responsible for the appearance of apparent naturally occurring anti-A and anti-K in the child's serum.

ABO Blood-Group System↗
PubMedDate not supplied

An anti-B reagent prepared from the alpha-D-galactopyranosyl-binding isolectins from Bandeiraea simplicifolia seeds.

A method for the large scale preparation of the alpha-D-galactosyl binding isolectins from Bandeiraea simplicifolia seeds using an absorbent prepared by linking D-galactosamine to CH-Sepharose is described. The addition of N-acetyl-D-galactosamine (GalNAc) to these isolectins produced an anti-B reagent (BS I + GalNAc anti-B). Although BS I + GalNAc anti-B readily agglutinated red blood cells from the majority of group B and AB donor and patient blood samples tested, it reacted weakly with group B and AB cord red blood cells and failed to agglutinate five of 100 group AB donor blood samples when tested by an automated technique. The reagent did not agglutinate the red blood cells from seven acquired-B red blood cell samples and was strongly reactive with Tn-polyagglutinable red blood cells. These findings indicate that this lectin anti-B preparation may be of more value in investigative immunohematology, rather than as an alternative to human group A serum as a source of anti-B for blood-typing purposes. The results of tests on Tn-polyagglutinable red blood cells with BS I + GalNAc anti-B and the purified isolectins BS I(A4) and BS I(B4) are also presented, and discussed in relation to current concepts on the structure of the Tn receptor.

ABO Blood-Group System↗
PubMedDate not supplied

Auto anti-Kpb associated with weakened antigenicity in the Kell blood group system: a second example.

An 84-year-old woman with intestinal bleeding had marked reduction of red blood cell antigenicity in the Kell system, and a positive direct antiglobulin test caused by auto-anti-Kpb. KX antigen activity of her cell was increased, an observation which supports the belief that KX marks a precursor structure utilized in the normal Kell biosynthetic pathway. It is postulated that reduced Kell antigenicity was an acquired change that resulted from enzymatic degradation, possibly of bacterial origin.

Adolescent↗