Biomedical subjects

S Ferrini

Publications and source records attributed to S Ferrini.

At least 109 records · Page 6Linked to original sources

PubMed1988

CD3-negative lymphokine-activated cytotoxic cells express the CD3 epsilon gene.

The expression of genes encoding different polypeptide chains of the TCR-CD3 complex was analyzed in a panel of cloned MHC-unrestricted cytotoxic cells. The clones were derived from CD3+ and CD3- human PBL. After expansion in rIL-2, all clones were able to lyse the NK-sensitive target cell line K562. In contrast, lysis of fresh tumor cells was achieved almost exclusively by CD3- clones. To test whether a known TCR-CD3 complex may be involved in MHC-unrestricted cytotoxicity, total RNA from nine CD3+ and 11 CD3- clones was isolated and hybridized with DNA probes for the TCR alpha-, beta-, and gamma-chains and for the CD3 gamma-, delta-, and epsilon-chains. TCR gamma transcripts were present at high levels in CD3+CD4- CD8- clones but were undetectable in all CD3- clones. Lysis of fresh tumor cells is an activity which can be independent of the TCR alpha beta and TCR gamma complexes because the CD3- clones did not express these TCR genes. Interestingly, all CD3- clones expressed CD3 epsilon transcripts, but not CD3 gamma- or delta-transcripts. CD3- lymphokine-activated cytotoxic cells may therefore be derived from immature T cells which do not yet express a complete CD3 complex. The CD3 epsilon chain, if expressed in CD3- cells in association with other molecules, could be involved in the activation and lytic function of these MHC-unrestricted cytotoxic cells.

Antigens, Surface↗

PubMed1988

Graves' disease: phenotypic and functional analysis at the clonal level of the T-cell repertoire in peripheral blood and in thyroid.

We have investigated at the clonal level the repertoire of intrathyroid and peripheral T lymphocytes in three patients with Graves' disease using a high efficiency cloning technique. Clonal efficiencies ranged from 10 to 31% for intrathyroid, and from 19 to 100% for peripheral T cells. In Graves' disease the phenotypic analysis showed similar percentages of CD3+ CD4+ CD8- and CD3+ CD4- CD8+ clones in thyroid infiltrates and peripheral blood. The functional evaluation showed similar or lower proportions of cytolytic clones in thyroid infiltrates with respect to peripheral blood. Furthermore, the proportions of intrathyroid and peripheral T-cell clones capable of releasing interleukin-2 and/or gamma-interferon in response to mitogen stimulation were similar. Finally, 44% of intrathyroid clones were neither cytolytic nor able to release IL-2 and gamma-interferon. These results are strikingly different from those obtained in Hashimoto's thyroiditis, where the large majority of intrathyroid T-cell clones are cytolytic and the proportions of clones able to release gamma-IFN are remarkably increased in thyroid infiltrates when compared to those obtained from peripheral blood. Taken together, these data suggest a different role for T lymphocytes in the pathogenesis of the two major human autoimmune thyroid diseases.

Adult↗

PubMed1987

Analysis of signal transducing mechanisms in CD3+ CD4- CD8- cells expressing the putative T cell receptor gamma gene product.

The signal transducing mechanisms, involved in the activation of CD3+ WT31- cells bearing the putative products of T cell receptor gamma genes, have been investigated. After stimulation with phytohemagglutinin or with monoclonal antibodies directed against CD2 or CD3 surface molecules, a rapid increase in free cytoplasmic Ca2+ concentration rise was detected in one representative CD3+ WT31- clone and in PEER cell line. Experiments performed in the presence of the Ca2+ chelator EGTA indicated that the free cytoplasmic Ca2+ concentration rise was consequent to an early release of Ca2+ from internal stores, followed by a sustained Ca2+ influx from the extracellular compartment. Moreover, increased levels of inositol-3-phosphate (the putative mobilizer of Ca2+ from the intracellular stores) were observed after stimulation, thus suggesting that activation of this cell subset occurs via the classical inositol-lipid metabolic pathway.

Antibodies, Monoclonal↗

PubMed1987

Phenotypic and functional analysis of human CD3+ and CD3- clones with "lymphokine-activated killer" (LAK) activity. Frequent occurrence of CD3+ LAK clones which produce interleukin-2.

Clones capable of lysing fresh, uncultured tumor cells ("lymphokine-activated killer": "LAK" activity) were selected from microcultures derived from either E-rosette-positive or E-rosette-negative cell populations. All the selected clones displayed a strong cytolytic activity against the NK-sensitive K562 cell line. Two major phenotypic groups of clones could be identified: a first group expressed the CD3 differentiation antigen, present exclusively on mature T lymphocytes; however, in contrast to typical cytolytic T lymphocytes, the majority of these clones expressed the unusual CD4- CD8- phenotype, whereas the remainder were CD4- CD8+. A second group was represented by CD3- clones which, in most instances, expressed the T-cell-lineage-specific CD2 antigen. Following stimulation with phytohemagglutinin (PHA), most of the CD3+ LAK clones produced Interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) whereas those expressing the CD3- phenotype did not. Since previous studies indicated that PHA may be inefficient in inducing lymphokine production by T-cell variants lacking the CD3/T cell receptor complex (TCR), CD3- clones were further stimulated with the calcium ionophore A23187 plus phorbol 12-myristate 13-acetate (PMA). Only 2/11 CD3- LAK clones produced small amounts of IL-2, whereas the majority released IFN-gamma. Given the peculiar phenotypic and functional properties of many CD3 + LAK clones, we suggest that they may belong to a T-cell subset distinct from typical CTLs.

Antigens, Differentiation, T-Lymphocyte↗

PubMed1987

A novel 120-kD surface antigen expressed by a subset of human lymphocytes. Evidence that lymphokine-activated killer cells express this molecule and use it in their effector function.

A human cell clone (SF-16) displaying strong cytolytic activity against fresh tumor target cells was used for production of murine mAbs against surface antigens expressed by lymphokine-activated killer (LAK) cells and their peripheral blood precursors. The preliminary screening of hybridoma supernatants was performed according to the ability to bind SF-16 cells. Selected mAbs were further analyzed for their reactivity with several T and B cell lines and with peripheral blood T and non-T cell populations. A selected mAb, termed anti-LAK-1, only reacted with some T cell lines and with 15-30% of PBMC. Approximately 10-15% E-rosetting (T) cells and 40-50% E-rosette-negative cells were LAK-1+, as determined by cytofluorometric analysis. As the fluorescence distribution of LAK-1 antigen was clearly bimodal, LAK-1+ and LAK-1- cells could be separated by FACS. Positive cells were composed of large granular lymphocytes (LGL), whereas negative cells were mostly small lymphocytes and monocytes without LGL. After culture in rIL-2, purified LAK-1+ (but not LAK-1-) cells acquired the ability to lyse NK-resistant fresh melanoma target cells. In addition, only the LAK-1+ fraction of PBMC cultured for 5 d in rIL-2 lysed fresh tumor targets, thus indicating that the LAK-1 antigen is expressed also on LAK effector cells. Unlike some other LGL/NK cell markers, LAK-1 antigen is characterized by a stable expression: thus, LAK-1+ cell populations cultured for up to 20 d in rIL-2 maintained the LAK-1 antigen expression, whereas HNK-1 and, partially, CD16 were lost. Finally the cytolytic activity of LAK effector cells generated from PBMC cultured for 3 d in rIL-2 was susceptible to inhibition by the anti-LAK-1 mAb.

Antibodies, Monoclonal↗

PubMed1987

Characterization of CD3+, CD4-, CD8- clones expressing the putative T cell receptor gamma gene product. Analysis of the activation pathways leading to interleukin 2 production and triggering of the lytic machinery.

Four clones were derived from human peripheral blood T lymphocytes from which CD4+ and CD8+ cells had been removed by treatment with specific mAbs and complement. All expressed the CD2+, 3+, 4-, 8-, T44- phenotype, and did not react with the WT31 mAb, which is specific for a framework determinant of the CD3-associated alpha/beta heterodimer which serves as receptor for antigen on most human T lymphocytes. Surface iodination followed by crosslinking with dithiobis-succinimidyl propionate (DSP) and immunoprecipitation with anti-CD3 mAbs indicated that, in all four clones, the CD3-associated molecules consisted of a major 45 kD band and a minor band of 43 kD. Northern blot analysis showed that mRNA for the gamma chain was expressed at high levels, whereas mRNA for the alpha chain was missing; beta chain mRNA was present in a defective form (1 kb instead of 1.3 kb). These data support the concept that these clones may express, in association with CD3, the molecular product of the T cell receptor gamma genes instead of the typical alpha/beta heterodimer. CD3+, WT31- clones lysed the NK-sensitive K562 target cells and produced IL-2 upon stimulation with PHA. In addition, they released IL-2 after triggering with soluble anti-CD3 mAbs or with an appropriate combination of anti-CD2 mAbs (in the presence of adherent cells). When CD3+, WT31- clones were incubated with an anti-CD3 producing hybridoma as triggering target, the latter was efficiently lysed. Target cell lysis also occurred when a suitable combination of anti-CD2 mAbs-producing hybridomas was used. Therefore, CD3+, WT31- cells appear to use two pathways of cell activation that function also in conventional CD3+, WT31+ T cells, but they lack a third putative pathway initiated by T44 surface molecules.

Antibodies, Monoclonal↗

PubMed1987

Phenotypic and functional characterization of recombinant interleukin 2 (rIL 2)-induced activated killer cells: analysis at the population and clonal levels.

In these studies we investigated the phenotypic and functional characteristics of human rIL 2-activated killer cells (LAK). By FACS sorting we separated PBL into Leu-11- and Leu-11+ cell fractions and cultured them for 4 days in 100 U/ml rIL 2. Under these culture conditions, cells of the Leu-11+ fraction acquired a stronger LAK activity against fresh autologous or allogeneic melanoma cells as compared with Leu-11- cells or unfractionated PBL. To better characterize the cells responsible for this cytolytic activity, we directly cloned Leu-11+ and Leu-11- FACS-sorted cells in the presence of 1% PHA, irradiated spleen feeder cells, and rIL 2. From 6 to 10% of the Leu-11+ cells and from 42 to 66% of the Leu-11- cells plated gave rise to clonal progenies that were tested simultaneously for cytolytic activity against fresh melanoma cells and NK-sensitive K562 target cells in a 4-hr 51Cr-release assay. Most of the Leu-11+ microcultures lysed fresh melanoma target cells (35 out of 38 and 26 out of 34 in two separate experiments), whereas only a few clones derived from the Leu-11- cell fraction had this capability (four out of 45 and one out of 41). All the clones lysing fresh melanoma cells also efficiently killed K562 target cells, whereas other clones lysing only K562 could be found among Leu-11+ and Leu-11- clones. Nine clones expressing LAK activity were tested for their reactivity against a panel of different tumor target cells. All clones were able to lyse a broad panel of target cells including NK-sensitive and NK-resistant cultured or noncultured human tumor target cells, as well as mouse tumor cell lines. Surface marker analysis of 14 clones displaying LAK activity, all derived from Leu-11+ cells, showed that they were all T3 (CD3)-, whereas 10 out of 14 expressed the T11 (CD2) antigen and only four were weakly stained by an anti-T8 (CD8) mAb. All 14 clones expressed the T40 (CD7) T cell marker and DR and LFA-1 antigens. Cytolysis inhibition experiments performed on a rIL 2-activated Leu-11+ population and on two LAK cell clones, both expressing T11 antigen, showed that anti-LFA-1 but not anti-T11 mAb could inhibit cytolysis of freshly derived tumor target cells.

Antibodies, Monoclonal↗

PubMed1987

Surface markers of human lymphokine-activated killer cells and their precursors. Analysis at the population and clonal level.

Lymphokine-activated killer (LAK) activity was first analyzed on PBL populations fractionated on the basis of the expression of T11 or T3 antigen. LAK cell precursors were found to be present in both T11+ and T11- populations, but only in the T3- cell fraction. The generation of LAK activity in highly purified T3- populations of PBL was not accompanied by expression of T3 antigen during a 5-day culture period. LAK activity was next analyzed at the level of limiting dilution clonal microcultures. T11+T3- and T11+T3+ cells, cloned under optimal culture conditions, gave a frequency of proliferating cells of approximately 1 cell in 1.25 for T11+T3+ and 1 cell in 10 for T11+T3- cells. Clones were screened for their ability to lyse fresh ovarian carcinoma cells and K562 target cells. The majority of LAK clones were derived from the T11+T3- cells; moreover, most of the clones derived from these cells displayed LAK activity. Clones displaying LAK activity lysed a panel of fresh or cultured tumor target cells, but failed to lyse PHA-activated lymphoblasts. Surface marker analysis indicated that all the clones had maintained the original T11/T3 phenotype. Whereas 2 T3+ selected LAK clones expressed the T8+T4- phenotype, only 1 out of 9 T3- clones was T8+T4-, all the others lacking both T4 and T8 antigens.

Antigens, Differentiation, T-Lymphocyte↗

PubMed1987

Human CD3+4-8-WT31- T lymphocyte populations expressing the putative T cell receptor gamma-gene product. A limiting dilution and clonal analysis.

The small peripheral blood CD3+ T cell population lacking both CD4 and CD8 surface antigens has been analyzed in the present study. Enriched CD3+4-8- populations were obtained by depletion with anti-CD4 or anti-CD8 monoclonal antibodies (mAb) and complement. The resulting populations contained greater than 99% CD2+ cells, whereas CD3+ represented approximately 50%. Virtually all of the cells were CD4-8- and did not react with the WT31 mAb, specific for a framework determinant of the alpha/beta T cell receptor (TCR). In order to analyze the molecular nature of CD3-associated molecules in CD3+WT31- populations, cells were stimulated with 0.5% phytohemagglutinin (PHA) for 24 h and expanded for an additional 7-14 days in interleukin 2 (IL 2). The resulting cells were greater than 95% CD3+ and expressed neither CD4/CD8 nor WT31 antigen. Cell surface iodination followed by cross-linking and immunoprecipitation with anti-CD3 mAb showed that CD3-associated molecules consisted of a major 45-kDa band and a minor band of 43 kDa. Thus, whereas CD3-associated molecules isolated from polyclonal CD3+WT31+ populations (expanded in IL 2 under the same culture conditions) appeared as diffuse bands, CD3-associated molecules isolated from CD3+WT31- populations displayed a homogeneous molecular mass. Northern blot analysis revealed the presence of mRNA for the TCR gamma chain whereas the mRNA for the alpha chain was mostly represented by a truncated (1.2 kb) form. Also small amounts of a nonproductive mRNA for the beta chain were detected. Freshly isolated CD3+WT31--enriched populations proliferated in response to PHA and concanavalin A, moreover, IL 2 was detected in the culture supernatants after cell stimulation. By applying culture conditions which allow virtually all T cells to undergo clonal expansion, approximately 1/3 CD3+WT31- were clonogenic. In addition, the large majority of proliferating microcultures lysed the K562 cell line and about half the natural killer (NK)-resistant fresh melanoma target cells. A large number of clones derived from CD3+WT31- enriched populations by limiting dilution has been further analyzed. More than 95% of the clones were CD3+4-8-WT31-; 12/15 clones analyzed in more detail displayed NK activity and 6/15 lysed melanoma cells; in addition, all lysed P815 target cells in the presence of PHA, thus indicating that all the clonogenic CD3+WT31- cells have a cytolytic potential.

Antibodies, Monoclonal↗

PubMed1987

Clonal analysis of T lymphocytes infiltrating the thyroid gland in Hashimoto's thyroiditis.

T cells isolated from thyroid tissue and peripheral blood of 2 patients with Hashimoto's thyroiditis were studied by a high cloning efficiency microculture technique. Clonal efficiencies of 37 and 24% were obtained from thyroid-derived T cell cultures, while 40 and 90% efficiencies resulted from peripheral-blood-derived cultures. A prevalence of T4-/T8+ T cell clones were found in thyroid infiltrates. The functional analysis of the clones demonstrated significantly higher proportions of clones with cytolytic activity in a lectin-dependent assay in thyroid-derived microcultures, as compared to peripheral blood-derived ones. The proportion of clones displaying natural-killer-like activity was increased in 1 patient only. Cytolytic activity was displayed not only by all T4-/T8+, but also by several T4+/T8- intrathyroid clones. Remarkable proportions of cytolytic clones were also able to release interleukin-2 upon phytohemagglutinin stimulation. Finally, the proportion of T cell clones able to release gamma-interferon following mitogen stimulation was significantly higher in thyroid- vs. peripheral-blood-derived microcultures. These results provide further data about the possible pathogenetical role of both regulatory and effector T lymphocytes in human autoimmune thyroiditis.

Adult↗

PubMed1986

Cyclosporin-A inhibits IL-2 production by all human T-cell clones having this function, independent of the T4/T8 phenotype or the coexpression of cytolytic activity.

Cyclosporin A (CsA) is an immunosuppressive drug that acts, at least in part, by blocking IL-2 release. Since IL-2-producing human T cells are heterogeneous with respect to their functional capabilities and surface phenotype, we investigated whether differences in sensitivity to CsA existed among different IL-2-producing T-cell clones. Preliminary dose/response experiments showed that 100 ng/ml CsA completely inhibited the PHA- or OKT3-induced IL-2 production by four representative T4+/T8- clones. On the other hand, this drug concentration had virtually no inhibitory effect on the proliferation of CTL-L murine indicator cells to exogeneous IL-2. Clones were derived directly from peripheral blood by applying a microculture system that allows clonal expansion of essentially all T cells: under these experimental conditions growing clones are therefore highly representative of the starting T-cell populations. Among clones so derived, 28 were selected according to their capability to release IL-2 upon PHA stimulation. Six of such clones displayed cytolytic activity in a PHA-dependent assay against P815 murine target cells. CsA (100 ng/ml) abrogated IL-2 production of all clones, including those displaying cytolytic activity and expressing the T4-/T8+ phenotype.

Clone Cells↗

PubMed1986

Effects of continuous low-level exposure to radiofrequency radiation on intrauterine development in rats.

To assess the effect of low-level radiofrequency radiation on pregnant rats, gravid dams were exposed continuously to 0.1 mW cm-2 at 27.12 MHz during different periods of pregnancy. Biological assays consisted of determining pre- and post-implantation losses and the effects on maternal body weight increase. Fetal parameters monitored included sex, mean viable fetal weight on Day 20 of gestation, external, skeletal and visceral fetal malformations, anomalies and variations. Dosimetric evaluations were made in terms of average specific absorption rate (SAR) and basal metabolic rate (BMR). Findings included a considerable increase in the percentage of total resorptions, reduced body weight increase in the exposed dams and incomplete cranial ossification in their fetuses. Results obtained were compared with those shown by other authors. It seems possible to ascribe some of the effects to a specific action of the radiofrequency radiation occurring independently of the rise in temperature. The hypothesis the exposure time, together with SAR, plays an important role in inducing specific exposure effects due to radiofrequency radiation is presented.

Abnormalities, Radiation-Induced↗

PubMed1985

Clonal analysis of T lymphocytes isolated from ovarian carcinoma ascitic fluid. Phenotypic and functional characterization of T-cell clones capable of lysing autologous carcinoma cells.

T lymphocytes isolated from ascitic fluid of patients with stage III-IV ovarian carcinoma were cloned by means of a microculture system that allows cloning of virtually all peripheral blood human T lymphocytes. Under these experimental conditions, 15% to 42% of ascitic T cells gave rise to clonal progenies that were analyzed for different functional capabilities. Of the clones obtained, 36%-70% had cytolytic activity in a PHA-dependent assay (using P815 as target cells) that allowed detection of cytolytic cells of any specificity. About one-half of the cytolytic clones lysed the NK-sensitive K562 target cells as well. In addition, 30%-50% of the total clones released IL-2 upon stimulation with PHA for 24 hr. In all patients analyzed a variable proportion (11%-56% of all cytolytic clones) had cytolytic activity against autologous tumor cells. Some of these clones have been analyzed in more detail: 18/21 expressed the T4-T8+ phenotype, whereas the remaining 3 were T4+ T8-. Only one out of 6 clones tested lysed allogeneic ovarian carcinoma cells as well, while 5/8 had a definite NK-like activity. Finally, all 8 clones tested were inhibited by anti-T11 and 7/8 by anti-T8 monoclonal antibody.

Antibodies, Monoclonal↗

PubMed1984

Incidence of T cell subset imbalance in relatives of Graves' disease patients.

In previous reports we demonstrated imbalances of T cell subsets in patients with autoimmune thyroid disease. In the present investigation, we studied several T cell markers with different functional meaning (Fc gamma-receptors, HLA-Ia antigens, MLR4 and 5/9 antigens) in first degree relatives of Graves' disease patients. Our data suggest that imbalances of circulating T cell subpopulations are apparent only when abnormal hormone levels and/or thyroid autoantibodies are present.

Adolescent↗

PubMed1984

Prolactin secretion in pubertal and adult male subjects.

Prolactin, LH and FSH circadian secretion were studied in a group of 20 boys in various pubertal stages and in 13 normal male adults. Prolactin 24-hour integrated concentration was similar in all groups except in stage 2 boys, in which it was significantly higher with respect to stage 3-4 boys. This pattern was observed also for nocturnal, but not for diurnal concentration. As already described by other authors, LH showed and amplified circadian secretion in stage 2 and 3-4 boys, particularly during night time. FSH increase was less evident, and reached the peak 24-hour mean concentration in stage 2 subjects. Our results suggest that during puberty the hypothalamic pituitary system increases its activity not only with regard to gonadotropins but also to prolactin secretion.

Adolescent↗

PubMed1984

Thyroglobulin-induced T-cell in vitro proliferation in Hashimoto's thyroiditis: identification of the responsive subset and effect of monoclonal antibodies directed to Ia antigens.

Recently it was reported that the peripheral blood and thyroid gland of patients with Hashimoto's thyroiditis contain activated (Ia+ and/or MLR4+) T cells and high levels of 5/9+ ("helper") T lymphocytes. In normal individuals the 5/9 monoclonal antibody recognizes a T-cell fraction that includes all T lymphocytes with inducer activities. Here, circulating 5/9+ and 5/9- T lymphocytes were isolated from patients with Hashimoto's disease, and the proliferative response induced by human thyroglobulin was investigated. The results show that the total thyroglobulin-induced lymphocyte DNA synthesis is confined to the 5/9+ T-cell fraction. Further subfractionation of 5/9+ into MLR4+ and MLR4- cells clearly indicates that no substantial differences exist in their proliferative capacities. Whether 5/9, MLR4, and Ia antigens, all expressed on the thyroglobulin-responsive T-cell subset, are involved in thyroglobulin-induced cell proliferation, was also analyzed. Although both 5/9 and MLR4 monoclonal antibodies had no effect, complete inhibition of antigen-induced blastogenesis was observed upon addition of monoclonal antibodies (D1/12 and BT2/9) directed to common determinants of Ia antigens. This inhibitory effect was also observed when T or non-T fractions were separately incubated with the monoclonal antibodies before culture. These results indicate that in humans, as in animals, the major histocompatibility complex may play a role in autoimmune thyroiditis. The data show that (a) the thyroglobulin-induced proliferative response is confined to a subset (5/9+) of T lymphocytes and (b) Ia antigens are involved in thyroglobulin-induced lymphocyte DNA synthesis in Hashimoto's disease.

Adult↗

PubMed1984

Deficiency of the autologous mixed lymphocyte reaction in patients with autoimmune thyroid disease.

The proliferative response of T lymphocytes when cocultured with autologous non-T cells in the absence of any other stimulating substance has been termed the autologous mixed lymphocyte reaction (AMLR). The AMLR has been shown to be impaired in several autoimmune disorders, such as systemic lupus erythematosus, Sjögren's syndrome, and primary biliary cirrhosis. In this study we report marked deficiency in the AMLR in two autoimmune disorders: Hashimoto's and Graves' diseases. This impaired AMLR, probably related to previously described T cell subset imbalances, provides further evidence of altered interactions between the immunocompetent cellular subsets in patients with these pathological conditions. Additional preliminary observations suggest defective allogeneic mixed lymphocyte reactions as well.

Adult↗

PubMed1984

Activation of T lymphocytes and autologous mixed lymphocyte reaction in allergic patients.

In allergic patients the authors previously observed high proportions of circulating T lymphocytes bearing Ia antigens, assumed to be "activated" T cells. In the present investigation they employed other T cell activation markers (4F2, insulin receptor, MLR4) which differ in the kinetics of appearance upon the surface of stimulated T cells. They report high proportions of Ia and 4F2-positive T cells, normal levels of MLR4-positive T lymphocytes and no insulin binding on T cells. However, T cells of allergic subjects are able to express insulin receptors in PHA-induced culture, such as normal subjects do. The authors conclude that these data, supported by similar observations in autoimmune diseases, indicates differences between in vivo and in vitro features of expression of T cell activation markers. In addition the autologous mixed lymphocyte reaction (AMLR) in atopic patients was studied. The results indicate that AMLR responsiveness is defective in allergic patients.

Adult↗