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Biomedical subjects

W L Marsh

Publications and source records attributed to W L Marsh.

At least 109 records · Page 6Linked to original sources
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

Antigens of the Kell blood group system on neutrophils and monocytes: their relation to chronic granulomatous disease.

KX, an antigen related to the Kell blood group system, is present in trace amounts on normal red cells and is strongly active on the neutrophils of all of 50 persons thus far tested. Normal circulating monocytes are now shown to also bear KX determinants. Absence of neutrophil KX has been associated with all of three previously tested patients with chronic granulomatous disease. In this study two male siblings with CGD also have been shown to have KX negative leukocytes, and white blood cells from their heterozygous mother were found to have a reduced competency to absorb anti-KX. Five CGD boys are known to lack KX; the probability of this occurring by chance is greater 10(-6).

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↗
PubMed1975

Demonstration of the Gerbich antigenic determinant on neutrophil leukocytes.

Leukocyte-platelet concentrates prepared from blood of Gerbich (Ge) positive donors possess the capability of absorbing anti-Ge. Leukocytes from Ge-negative donors do not absorb the antibody, thus confirming the Ge antigen specificity. Tests with separated leukocyte types suggest that the Ge antigen is present on neutrophils and possibly monocytes, but absent from lymphocytes and platelets.

Absorption↗
PubMed1975

The Duffy blood group system: a review of recent developments.

Five antigenic specificities are associated with the Duffy blood group system. Fya, Fyb, By3 and Fy4 are under the genetic control of a locus near the centromere of chromosome 1. Fy5 is absent from Fy (a-b-) red cells and also from cells that have the Rhnull phenotype. It appears that interaction between Duffy and Rh gene products may be necessary for synthesis of Fy5 antigen. Most Caucasians have a Fya or Fyb gene (or both), inherited by strict Mendelian principles. No evidence has been found to suggest that independently segregating Duffy modifying genes exist. The frequency of Duffy genes varies greatly in different sections of the world population. Aboriginal populations have a high frequency of Fya, Fyb is the most common gene in European Caucasians, and Negroes have a high frequency of an allele named Fy. Anti-Fya is the most common Duffy antibody and is found most frequently in the serum of Caucasians immunized by blood transfusion. The Fya antigen is about 40 times less immunogenic than K antigen of the Kell system. Only about one anti-Fyb serum is found foe every 20 that are anti-Fya. The Fya and Fyb red cell antigen receptors are inactivated by proteolytic enzymes but not by neuraminidase. Sialic acid does not appear to be an essential component of the antigen structure. Duffy antigens appear to be thermolabile membrane proteins and they are not present in a soluble form in plasma or in body secretions.

Antibody Formation↗
PubMed1975

Present status of the Duffy blood group system.

In 1950 a new blood group antibody was recognized in the serum of a multi-transfused hemophiliac patient. The reactive red-cell antigen was identified in 65% of random caucasians, and the systemic name Duffy was proposed. Two common antigens, Fy-a and Fy-b, were recognized and shown to be products of autosomal allelic genes, but the great majority of negro individuals were found to lack both antigens. In 1968 genetic studies showed Duffy to be linked to Un-1, which is an inherited structural variation of chromosome number 1. Duffy thus became the first autosomal blood group gene to be allocated to a specific chromosome. Recent studies have allowed recognition of three new antibodies (anti-Fy3, anti-Fy4, and anti-Fy5) in the Duffy system. The Rh blood group locus has also been assigned to chromosome 1, and there is evidence that the antigen defined by anti-Fy5 is a product of interaction between Duffy and Rh genes. The Duffy blood group appears to be one of importance in clinical blood transfusion practice, and possibly makes the greatest distinction of any of the red cell systems between different groups of the world population.

Anthropology↗
PubMed1974

Mapping human autosomes: evidence supporting assignment of rhesus to the short arm of chromosome No. 1.

Rh-negative erythrocytes were found in the blood of an Rh-positive man suffering from myelofibrosis. Nucleated hemopoietic precursors were also circulating in his blood, and these cells had an abnormal chromosome complement from which identifiable chromosome segments had been deleted. Correlation of the serological and cytogenetic findings, combined with previous data, indicates that the Rhesus blood group locus is on the distal portion of the short arm of chromosome No. 1.

Chromosome Aberrations↗