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Biomedical subjects

H E Prince

Publications and source records attributed to H E Prince.

At least 19 recordsLinked to original sources
PubMed1997

Elevated CD38 antigen expression on CD8+ T cells is a stronger marker for the risk of chronic HIV disease progression to AIDS and death in the Multicenter AIDS Cohort Study than CD4+ cell count, soluble immune activation markers, or combinations of HLA-DR and CD38 expression.

The prognostic value of several immunologic markers were compared in Los Angeles Multicenter AIDS Cohort Study (MACS) participants, most of whom had been infected with HIV for >8 years. Markers studied included CD4+ cell number, flow cytometric measurements of CD8+ cell expression of CD38 and HLA-DR antigens, and serum markers of immune activation including neopterin, beta2-microglobulin, soluble interleukin-2 receptor, soluble CD8, and soluble tumor necrosis factor receptor-alpha (TNF-alpha) type II. Cox proportional hazards models indicated that elevated CD38 on CD8, a flow cytometric measurement of CD8+ T-lymphocyte activation, was the most predictive marker of those studied for development of a clinical AIDS diagnosis and death. As compared with the reference group, who had CD38 on CD8 <2470 molecules per CD8+ cell and in whom 4 of 99 developed clinical AIDS within 3 years, participants with CD38 on CD8 between 2470 and 3899, 3900 and 7250, and >7250 had relative risks (and numbers developing AIDS within 3 years) of 5.0 (15 of 81), 12.3 (24 of 60), and 41.4 (36 of 49), respectively. The strong prognostic value of CD38 on CD8 measurements and the fundamental importance of chronic immune activation in the pathogenesis of HIV disease suggests that this marker might have utility in the clinical management of HIV-infected persons.

ADP-ribosyl Cyclase↗
PubMed1997

Preferential replication of HIV-1 in the CD45RO memory cell subset of primary CD4 lymphocytes in vitro.

The ability of HIV-1 to establish an infection and replicate to high copy number in CD4 lymphocytes is dependent on both the activation state of the cell and virus-encoded regulatory proteins that modulate viral gene expression. To study these required virus-cell interactions, we have used an in vitro cell model of acute HIV infection of quiescent, primary CD4 lymphocytes and subsequent induction of T cell activation and virus replication by lectin or CD3 receptor cross-linking. Experiments were done to determine if the capacity of HIV to establish infection and complete replication was impacted by the maturational state of the CD4 cell target or the specific signal induction pathway engaged during activation. Primary CD4 cells were FACS-sorted into the major phenotypic subsets representative of memory (CD45RO) and naive (CD45RA) cells. Levels of virus replication were compared between infection with wild-type NL4-3 virus and an isogenic mutant containing a deletion in nef regulatory gene. PHA mitogen stimulation was compared with anti-CD3, with and without anti-CD28 costimulation, for induction of cell proliferation and virus replication. In both infected and uninfected cells, the RA cell subset exhibited significantly greater response to CD3/CD28 stimulation than did the RO cell subset. In contrast, the majority of virus replication occurred consistently in the RO cell subset. Deletion of HIV nef function caused a severe reduction in viral replication, especially in the RA naive cell subset after CD3 induction. PCR analysis of viral DNA formation, during infection of quiescent cells, demonstrated that the observed differences in HIV replication capacity between RO and RA cell subsets were not due to inherent differences in cell susceptibility to infection. Our results indicate that HIV replication is enhanced selectively in CD45RO memory phenotype cells through the probable contribution of specialized cellular factors which are produced during CD3-initiated signal transduction.

CD4-Positive T-Lymphocytes↗
PubMed1997

CD69 expression reliably predicts the anti-CD3-induced proliferative response of lymphocytes from human immunodeficiency virus type 1-infected patients.

Published studies suggest that mitogenic responses of lymphocytes can be reliably assessed by monitoring the expression of lymphocyte surface CD69 after 24 h of culture with the stimulant. We tested this hypothesis by determining the ability of lymphocyte CD69 expression to predict the outcome (normal or abnormal) of lymphocyte proliferative responses to anti-CD3 in a group of human immunodeficiency virus type 1 (HIV-1)-infected patients (n = 47). Cutoff values for defining normal and abnormal CD69 expression and proliferative ([3H]thymidine incorporation) responses were established with lymphocytes from healthy uninfected controls (n = 20). Lymphocytes from 29 HIV-infected patients exhibited an abnormal proliferative response, and those from 25 of the 29 also exhibited abnormal CD69 expression (sensitivity, 86.2%). Similarly, lymphocytes from 18 HIV-infected patients exhibited a normal proliferative response, and those from 16 of the 18 also exhibited normal CD69 expression (specificity, 88.9%). The predictive value of a normal CD69 result was 80%, and the predictive value of an abnormal CD69 result was 92.6%. These findings demonstrate that HIV-1-associated impairments in lymphocyte activation can be reliably detected by the rapid and nonradioactive CD69 expression assay.

Antigens, CD↗
PubMed1996

How many gated lymphocytes are needed for accurate assessment of T-subset percentages by flow cytometry?

Current regulatory agencies specify the use of 2,500 gated lymphocytes for accurate lymphocyte immunophenotyping by flow cytometry. However, acquisition of 2,500 gated lymphocytes is often technically infeasible when testing whole blood from lymphopenic patients. Our laboratory thus compared CD3, CD4, and CD8 percentages obtained from a lymphocyte acquisition gate of 2,500 events with those obtained, respectively, from 1,000 and 500 event acquisition gates. The study group consisted of 59 specimens with CD4 values ranging from 1% to 66%; for data analysis purposes, the group was considered as a whole and was then subdivided according to CD4 percentage (> 25%, < 25%, < 5%). For all groupings analyzed, percentages of CD3+, CD4+, and CD8+ lymphocytes were not significantly different for either 1,000-event or 500-event gates when compared to the standard 2,500 gate (paired t-test). Replicate parallel analyses of some samples indicated that comparable precision is obtained by using the alternative gates. These findings indicate that the use of smaller numbers of acquired lymphocytes is a reasonable alternative in situations where 2,500 lymphocytes cannot be attained.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Costimulatory effects of T cell proliferation during infection with human T lymphotropic virus types I and II are mediated through CD80 and CD86 ligands.

The modulation of expression of CD80 and CD86 on T cells following infection with human T lymphotropic virus (HTLV)-I/II and its functional importance in T-T cell interactions was examined. Infection with HTLV-I/II leads to constitutive expression of CD80 and CD86, concomitant to down-modulation of CD28 on T cells. The CD80/CD86+ HTLV-infected T cells stimulated proliferation of allogeneic and autologous resting T cells, which could be specifically blocked by a soluble CTLA-4Ig chimeric protein, anti-CD80 or anti-CD86, but not by anti-CD54. It was necessary to inhibit interaction with both ligands (CD80 and CD86) to optimally block HTLV-mediated proliferation of allogeneic and autologous resting T cells. Simultaneous addition of anti-CD8O and anti-CD86 Abs also inhibited production of IFN-gamma, TNF-alpha, and IL-4, with no effect on IL-10 production, for both allo- and autologous T cell proliferation. Further, there was a direct correlation between the spontaneous proliferation of lymphocytes from patients infected with HTLV-II and expression of CD80, which could be blocked by simultaneous addition of anti-CD80 and anti-CD86. Taken together, these results suggest that HTLV-infected CD80/CD86+ T cells serve as APCs, leading to a sustained proliferation of T cells, and that both ligands participate in allostimulation, autologous proliferation, as well as spontaneous proliferation of HTLV-II-infected PBMC.

Adult↗
PubMed1995

Influence of specimen age and anticoagulant on flow cytometric evaluation of granulocyte oxidative burst generation.

The oxidative burst generation capacity of granulocytes can be reliably detected by a flow cytometric procedure using lysed whole blood, dihydrorhodamine 123 (DHR), and phorbol myristate acetate (PMA). This assay is used to detect chronic granulomatous disease (CGD) and the CGD carrier state. To assess the feasibility of performing this assay in a reference laboratory setting, we investigated the influence of anticoagulant and specimen age on flow cytometric detection of granulocyte oxidative burst generation. Peripheral blood from 20 healthy controls was collected in acid citrate dextrose (ACD), ethylenediaminetetraacetate (EDTA), or sodium heparin (HEP) and held at room temperature. At 4, 24, 48, 72, and 96 h after collection, red cells were lysed, the white cells loaded with DHR, and then activated by PMA. Granulocyte-associated fluorescence, indicative of oxidative burst generation, was assessed by flow cytometry. Blood in any of the three anticoagulants tested gave reliable results (> 90% of granulocytes positive for fluorescence) at 4 h after collection; at 24 h after collection, HEP and ACD specimens performed slightly better than EDTA specimens. At later time points, HEP proved superior to ACD and EDTA for maintaining granulocyte oxidative burst capacity. As a demonstration of the practical utility of the assay, both CGD and the CGD carrier state were accurately detected using heparinized blood specimens analyzed 72 h after collection. These results show that heparinized blood specimens up to 72 h old can be used to reliably assess granulocyte oxidative burst generation.

Anticoagulants↗
PubMed1995

Spontaneous proliferation of memory (CD45RO+) and naive (CD45RO-) subsets of CD4 cells and CD8 cells in human T lymphotropic virus (HTLV) infection: distinctive patterns for HTLV-I versus HTLV-II.

Spontaneous lymphocyte proliferation (SLP) in vitro is a characteristic feature of about 50% of individuals infected with HTLV-I or HTLV-II. Both CD4 cells and CD8 cells contribute to SLP in HTLV-I infection, whereas SLP in HTLV-II infection is usually restricted to CD8 cells. In this study, we asked if SLP was restricted to the memory (CD45RO+) cell subset of CD4 and CD8 cells in HTLV infection. Purified CD4 and CD8 cells were separated into CD45RO+ and CD45RO- populations by a modified panning technique, and spontaneous proliferation (SP) of the cell subsets was assessed. For all five HTLV-I-infected persons whose mononuclear cell cultures were SLP+, only CD45RO+ cells, but not CD45RO- cells, within CD4 and CD8 subsets showed SP. In contrast, five of six SLP+ HTLV-II+ individuals showed SP in both the CD45RO+ and the CD45RO- subsets of CD4 cells, and 10 of 12 SLP+ HTLV-II+ individuals showed SP of both the CD45RO+ and CD45RO- subsets of CD8 cells. Polymerase chain reaction studies showed that proviral genome was generally present in both CD45RO+ and CD45RO- subsets of CD4 and CD8 cells, regardless of HTLV type and SP activity. These findings show that SP of both CD4 and CD8 cells in HTLV-I infection is usually restricted to CD45RO+ memory cells, whereas in HTLV-II infection, both CD45RO+ memory and CD45RO- naive subsets of CD4 and CD8 cells may exhibit SP. It thus appears that HTLV-I infection and HTLV-II infection exhibit distinctive dysregulatory effects on memory and naive T cell subpopulations.

CD4-Positive T-Lymphocytes↗
PubMed1994

Reduction of escapee formation in flow cytometric analysis of lymphocyte subsets.

Most experienced flow cytometrists performing immunophenotyping of lymphocyte subsets are aware of the escape phenomenon, in which some positive cells are found outside a lymphocyte gate based on forward and right angle scatter. However, little information is available on the levels of escapees formed with different antibodies, the roles of fluorochromes and lysing agents, the mechanism explaining the phenomenon, or methods to reduce it. We thus performed a systematic analysis of the escapee phenomenon to clarify these issues. A panel of monoclonal antibodies, including a phycoerythrin (PE) conjugate and a fluorescein isothiocyanate (FITC) conjugate of the same antibody from one manufacturer, was used to treat whole blood specimens, after which red cells were lysed using 0.15 M ammonium chloride (AmChl). The percentages of gated lymphocytes expressing CD3, CD8, CD19, and HLA-DR, but not CD2, CD4, CD16, and CD25, were significantly lower in FITC-stained versus PE-stained preparations. Correlated analysis of green fluorescence and forward scatter showed that, on average, 18% of CD3+ events, 24% of CD8+ events, and 25% of CD19+ events were escapees when using the FITC conjugate. In dual color analysis, CD3+ escapees were positive for CD62-P, CD13, and CD14, indicating that the escapee events consisted of FITC-anti-CD3-coated lymphocytes complexed with platelet-coated myeloid cells. In studies of the role of lysing agent, essentially no escapees were found in specimens treated with FACS lysing solution, which contains formaldehyde. We therefore included a similar denaturing agent, paraformaldehyde (0.1%), in the AmChl lysing agent, and found that the occurrence of escapees was markedly reduced. These findings show that the escapee phenomenon occurs when using some FITC-conjugated monoclonal antibodies in conjunction with AmChl lysing agent, and can be reduced by inclusion of paraformaldehyde in the lysing agent.

Ammonium Chloride↗
PubMed1994

Screening of blood donors for idiopathic CD4+ T-lymphocytopenia.

BACKGROUND: The recent recognition of idiopathic CD4+ T-lymphocytopenia (ICL) had led to concern that an unknown immunodeficiency virus may be transmissible by transfusion. STUDY DESIGN AND METHODS: To evaluate the prevalence and significance of low CD4+ values among blood donors, CD4+ data on 2030 blood donors who were negative for antibody to human immunodeficiency virus type 1 (HIV-1) were compiled. Those with CD4+ values below ICL cutoffs (< 300 CD4+ T cells/microL, or < 20% CD4+ T cells) were recalled for follow-up investigations. Serial CD4+ data on 55 homosexual men who seroconverted during prospective follow-up and data on 139 anti-HIV-1-positive blood donors initially evaluated in 1986 were reviewed as well. RESULTS: Five seronegative donors (0.25%) had absolute CD4+ counts < 300 cells per microL and/or < 20 percent. On follow-up, all five donors had immunologic findings within normal ranges, lacked HIV risk factors, and tested negative for HIV types 1 and 2 and human T-lymphotropic virus type I and II infections by antibody and polymerase chain reaction assays. Four of five donors reported transient illness shortly after their low CD4+ count donations. The median interval from HIV-1 seroconversion to an initial CD4+ value below ICL CD4+ cutoffs was 63 months for infected homosexual men. Of 139 HIV-1-infected blood donors studied 1 to 2 years after seropositive donations, 34 (24%) had CD4+ counts < 300 cells per microL and/or < 20 percent. CONCLUSION: Low CD4+ counts are rare among anti-HIV-1-negative volunteer blood donors and are generally associated with transient illnesses. If any unknown virus progresses similarly to HIV-1, CD4+ count donor screening would be a poor surrogate for its detection.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Spontaneous lymphocyte proliferation in human T-cell lymphotropic virus type I (HTLV-I) and HTLV-II infection: T-cell subset responses and their relationships to the presence of provirus and viral antigen production.

Spontaneous lymphocyte proliferation (SLP) during in vitro culture of mononuclear cells (MCs) characterizes over half of asymptomatic individuals infected with human T-cell lymphotropic virus type I (HTLV-I) or HTLV-II. Both CD4 and CD8 T-cell subsets within MC cultures are activated during SLP, as judged by high-density CD25 (CD25bright) expression; it is unclear, however, whether both cell subsets can directly undergo SLP. In the present investigation, the SLP capacities of purified CD8 and CD4 cells were examined in subjects infected with HTLV-I (n = 19) or HTLV-II (n = 54) in relation to the SLP status of MCs from each subject. No increase in SLP was observed for CD8 or CD4 cells from SLP-negative (SLP-) HTLV-infected subjects, whereas robust SLP characterized CD8 cells from all SLP-positive (SLP+) individuals, regardless of HTLV type. In contrast, SLP+ CD4 cells characterized only 23% (7 of 31) of HTLV-II+ SLP+ individuals, whereas SLP+ CD4 cells characterized 100% of HTLV-I+ SLP+ individuals. In cocultures of HTLV-II+ SLP+ CD8 cells and autologous SLP- CD4 cells, sizable proportions of both CD8 cells and CD4 cells coexpressed CD25bright, suggesting that SLP- CD4 cells were activated in the presence of SLP+ CD8 cells. PCR analysis for tax sequences detected provirus in most CD4- and CD8-cell preparations from HTLV-seropositive individuals, regardless of type and the SLP status of cell subsets. To determine whether SLP was associated with activation of viral genes, levels of HTLV-I and HTLV-II core antigen (Ag) in supernatants were measured. Viral Ag production and SLP responses were significantly correlated for both CD4 and CD8 cells in both HTLV-I and HTLV-II infections. However, inhibition of CD8- or CD4-cell SLP by cyclosporin A or anti-Tac (anti-CD25) did not reduce Ag production, indicating that Ag production is not coupled to SLP. These findings show that CD4 cells from SLP+ HTLV-I+ and SLP+ HTLV-II+ individuals differ in SLP capacity, that the absence of SLP does not indicate a lack of infection, and that production of viral Ag is associated with, but not dependent on, SLP.

Base Sequence↗
PubMed1994

Characterization of circulating CD4+ CD8+ lymphocytes in healthy individuals prompted by identification of a blood donor with a markedly elevated level of CD4+ CD8+ lymphocytes.

During flow cytometric analysis of lymphocytes from healthy donors, we identified a donor (donor A) with 22% CD4+ CD8+ cells (versus values of < 4% for 65 other controls). To determine if CD4+ CD8+ cells from donor A and other controls were similar, we first defined the phenotypic profile of control CD4+ CD8+ cells. Enriched CD4+ CD8+ cell populations for 10 controls were prepared by a two-step positive selection scheme with anti-CD4-coated magnetic beads and anti-CD8-coated culture flasks; the selected population averaged 69% CD4+ CD8+ cells and 31% CD4+ CD8- cells. For all 10 controls, two subsets of CD4+ CD8+ cells, CD4dim CD8bright and CD4bright CD8dim, were observed. Phenotypic profiles of these two CD4+ CD8+ subsets were defined by pairing anti-CD8 with other monoclonal antibodies, and the profiles were compared with each other and with those of CD4+ CD8-, CD4- CD8bright, and CD4- CD8dim cells. CD8bright and CD4bright CD8dim cells differed in their proportions of CD62-L+ cells and in their levels of CD11a and CD2 expression. Both CD4+ CD8+ subsets resembled CD4+ CD8- cells in CD45RA, CD45RO, and CD25 expression; the comparable CD- CD8+ cells in CD62-L expression; and CD4- CD8bright cells in CD11b, CD11b, CD16/56, and CD28 expression. CD38 expression in both CD4+ CD8+ subsets was decreased compared with those of other cell subsets. Whereas control CD4+ CD8+ cells averaged 33% CD4dim CD8bright, CD4+ CD8+ cells from donor A were > 90% CD4dim CD8bright. Donor A CD4dim CD8bright cells exhibited proportional decreases in CD25 and CD62-L expression and increases in CD11b and CD54 expression compared with those of control CD4dim CD8bright cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Donors↗
PubMed1993

Preparation of CD8bright and CD8dim lymphocyte populations using two positive selection methods in tandem.

Two positive selection methods were compared for the ability to capture both the bright and dim subsets of CD8 lymphocytes in mononuclear cell (MC) preparations from ten healthy individuals. The first method utilized anti-CD8-coated magnetic beads; captured cells were then recovered using a polyclonal sheep anti-mouse Fab reagent. At all bead: CD8 cell ratios tested (4:1, 8:1, 16:1), the selected cells were > 94% CD8+, and these CD8 cells were enriched for CD8bright cells (77-85%) when compared to CD8 cells in the starting MC preparation (68%). The second method utilized anti-CD8-coated culture flasks; captured cells were recovered by physical dislodgement. The recovered cells were > 90% CD8+, and these CD8 cells were modestly enriched for CD8dim cells (52%) compared to starting CD8 cells (32%). To further enrich for CD8dim cells, we used these two methods in tandem (n = 10). MC were first incubated with anti-CD8-coated magnetic beads (4:1 ratio) to obtain a CD8bright-enriched population (97% of all cells CD8+, 83% of all cells CD8bright). Uncaptured cells were incubated with anti-CD4-coated magnetic beads, and the uncaptured cells from this step were then placed in an anti-CD8-coated flask. The recovered flask-selected cell population was highly enriched for CD8dim cells (87% of all cells CD8+, 85% of all cells CD8dim). CD8 cells in the CD8bright population were 94% CD3+ and 6% CD16+, whereas those in the CD8dim population were 29% CD3+ and 66% CD16+. In proliferative studies, CD8bright cells were preferentially activated by immobilized anti-CD3, whereas CD8dim cells were preferentially activated by exogenous IL-2. In assays of natural killer activity, CD8dim cells were markedly more active than CD8bright cells. This method provides an alternative to cell sorting for obtaining enriched populations of CD8bright and CD8dim lymphocytes.

CD8 Antigens↗
PubMed1993

The effect of methyldopa and procainamide on suppressor cell activity in relation to red cell autoantibody production.

Kirtland et al (1980) suggested that methyldopa caused the production of red cell (RBC) autoantibodies by causing a persistent increase in lymphocyte cyclic AMP, which inhibited suppressor T cell function, leading to unregulated autoantibody production in some patients. They showed that significantly higher lymphocyte cyclic AMP concentrations were generated by lymphocytes from healthy donors after adding methyldopa, and by lymphocytes from patients who were receiving methyldopa compared to lymphocytes from healthy donors without methyldopa present. They also showed that methyldopa affected suppressor cell activity. We measured the effect of methyldopa and procainamide on suppressor cell activity, using a similar approach to Kirtland et al (1980). Suppressor cell activity was measured by measuring the amount of IgG, produced in vitro, by B cells following mitogen stimulation preceded by a 24 h incubation period. We found no significant increase in the amount of IgG generated by normal donor lymphocytes, when methyldopa or procainamide was present during the preincubation period. This is in contrast to the findings of Kirtland et al (1980). We also measured the amount of IgG generated in vitro by mitogen-stimulated lymphocytes from patients (with and without positive direct antiglobulin tests) taking methyldopa and compared this to the amount of IgG generated by lymphocytes from normal donors and patients (with and without positive direct antiglobulin tests). The results were similar for each group. This does not agree with the findings of Kirtland et al (1980) who found that lymphocytes from patients taking methyldopa produced more IgG in vitro than lymphocytes from normal donors. Our results do not support the hypothesis that methyldopa and procainamide induce autoantibodies by affecting suppressor cell function.

Autoantibodies↗
PubMed1993

Modulatory effects of plasma and serum on T lymphocyte activation: distinctive patterns for different mitogens.

Published reports have shown that fresh plasma, but not cryoprecipitate-depleted plasma or fresh serum, inhibits T cell activation by phytohemagglutinin (PHA). We sought to determine if this pattern of inhibition also characterized T cell responses to mitogens differing from PHA with regard to the cell surface molecules utilized for signal transduction. The activation system included colchicine, which limits the cells to one round of division, masking stimulatory factors that enhance proliferation by boosting the number of divisions per culture period. A distinctive modulatory pattern characterized T cell responses to each of 4 mitogens tested (PHA, anti-CD3 monoclonal antibody, desialyzed oxidized erythrocytes (DOE), pokeweed mitogen). Enhanced proliferative responses to anti-CD3 and DOE were observed in the presence of serum, and reflected an increased percentage of T cells expressing CD25. These findings suggest that concerns regarding a negative impact of plasma components on T cell responsiveness, when based on results from PHA-induced activations systems, may be unwarranted.

Antibodies, Monoclonal↗
PubMed1992

Phenotypic comparison of the three populations of human lymphocytes defined by CD45RO and CD45RA expression.

Published reports indicate that CD45RO-CD45RAbright T cells are native T cells, CD45RObrightCD45RA- T cells are memory T cells, and that concomitant loss of CD45RA expression and gain of CD45RO expression occurs during transition from naive to memory status. Thus, following in vitro activation of CD45RO- CD45RAbright T cells, a subset of transitional CD45ROdimCD45RAdim T cells is observed before conversion to a CD45RObrightCD45RA- phenotype is completed. Interestingly, all three of these phenotypic subsets are represented in the circulating human lymphocyte pool. We thus used dual-color flow cytometry to phenotypically characterize CD45RObrightCD45RA-, CD45ROdimCD45RAdim, and CD45RO- CD45RAbright lymphocytes. Both the CD45RObrightCD45RA- and CD45ROdimCD45RAdim subsets consisted almost entirely of T cells, whereas the CD45RO-CD45RAbright subset contained T cells plus essentially all of the B and natural killer cells. Additional studies used three-color flow cytometry to assess activation markers on T cells within the three subsets defined by CD45RO/CD45RA expression. CD25 expression increased with conversion from naive to memory status (5% of CD45RO-CD45RAbright, 24% of CD45ROdimCD45RAdim, and 42% of CD45RObrightCD45RA- T cells), whereas CD38 expression decreased during conversion (76, 53, and 27%, respectively). We also assessed the fluorescent intensities of CD11a, CD2, and CD44, shown by others to be increased on memory, compared to naive T cells. Visual inspection of fluorescence cytograms confirmed these findings, and further showed that transitional T cells express these markers at levels indistinguishable from those for naive T cells. These findings suggest that acquisition of CD25 and loss of CD38 occur relatively early in the naive-to-memory transition process, being evident in the transitional cell subset. In contrast, increased expression of CD11a, CD2, and CD44 appear to represent late events, occurring after loss of CD45RA and gain of CD45RO has been completed.

Humans↗
PubMed1992

Lymphocyte subsets in HTLV-II-infected former blood donors: relationship to spontaneous lymphocyte proliferation.

Previous studies showed that over 70% of HTLV-seropositive blood donors from the Los Angeles area are infected with HTLV-II; further, mononuclear cells from about half of these HTLV-II+ donors exhibit spontaneous lymphocyte proliferation (SLP) during in vitro culture. To determine if HTLV-II+SLP+ donors exhibit more marked immune system changes than HTLV-II+SLP- donors, lymphocyte subsets for these two HTLV-II+ groups were compared to an uninfected control group. The percentage of lymphocytes expressing CD3 was significantly increased and the percentage expressing a CD16/56+CD3- phenotype (natural killer cells) was significantly decreased in the HTLV-II+SLP+ group (N = 34) versus the control group (N = 49). On the basis of absolute numbers, the lymphocyte number was significantly higher in the HTLV-II+SLP+ group than in the control group and reflected significant increases in the numbers of both CD4 and CD8 subsets of T cells. Analysis of proportional changes in CD4 and CD8 cell subsets revealed significant increases in the proportions of CD4 cells expressing HLA-DR, CD8 cells expressing HLA-DR, and CD8 cells expressing CD45RO for the HTLV-II+SLP+ group versus the control group. For all phenotypic parameters measured, no significant differences were noted when comparing the HTLV-II+SLP- group (N = 21) and the control group. Cell culture experiments utilizing purified CD4 cells and CD8 cells from a subset of each study group revealed that in vitro spontaneous proliferative capacity resides within both the CD4 cell and CD8 cell populations from SLP+ individuals. These findings show that changes in circulating lymphocyte subsets in HTLV-II infection are found only in association with SLP, and that the capacity to exhibit SLP characterizes both CD4 and CD8 lymphocyte subsets.

Blood Donors↗