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Monoclonal antibody‐defined T‐cell phenotypes and phytohemagglutinin reactivity of E‐rosette‐forming circulating lymphocytes from untreated chronic myelocytic leukemia patients
Author(s) -
Velardi Andrea,
Rambotti Pietro,
Cernetti Cristina,
Spinozzi Fabrizio,
Gerli Roberto,
Martelli Massimo F.,
Davis Stephen
Publication year - 1984
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19840215)53:4<913::aid-cncr2820530416>3.0.co;2-m
Subject(s) - monoclonal antibody , rosette (schizont appearance) , immunology , antigen , population , t lymphocyte , medicine , myelocytic leukemia , antibody , leukemia , lymphocyte , t cell , phenotype , microbiology and biotechnology , biology , immune system , biochemistry , environmental health , gene
T‐cell phenotypes, as defined by murine monoclonal antibodies, (OKT 3 , OKT 4 , OKT 8 , OKIaI), and phytohemagglutinin (PHA) reactivity, were evaluated in E‐rosette forming cells (T‐cells) from 10 untreated chronic myelocytic leukemia patients. The proportion of T 4 + cells was lower in patients than in controls (41.6 versus 61.7%, P < 0.02); whereas the proportion of T 8 + cells was similar in patients and controls. The decrease in T 4 + cells in CML resulted in a decrease in circulating T 4 + /T 8 + ratio ( P < 0.02). The la1 + T‐cells were increased in most CML (8 of 9) patients, white control subjects never displayed la1 + T‐lymphocytes ( P < 0.01). The PHA reactivity of E‐rosette forming lymphocytes was significantly impaired in CML patients with respect to controls ( P < 0.02). The presence of la antigen on T‐cells was positively correlated with the T 8 + cell phenotype ( P < 0.001) and inversely correlated with the T 4 + (helper) cell phenatype ( P < 0.05). Furthermore, there was a trend towards an inverse correlation between the PHA response and the level of lal + or T 8 + cells, there is no correlation between PHA reactivity and T 4 + phenotype. The results suggest that the T‐lymphocyte population from untreated CML patients is intrinsically abnormal.