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J B Winfield

Publications and source records attributed to J B Winfield.

At least 55 records · Page 3Linked to original sources
PubMed1988

Autoantibodies to the constitutive 73-kD member of the hsp70 family of heat shock proteins in systemic lupus erythematosus.

Serum from patients with systemic lupus erythematosus (SLE) frequently contain IgM and IgG autoantibodies to the constitutively expressed 73-kD/pI 5.5 member of the hsp70 family of heat shock proteins, as determined by one-dimensional (SDS-PAGE) and two-dimensional (IEF/SDS-PAGE) immunoblotting, and by solid-phase SLE Ig immunoprecipitation experiments using hsp70 protein-specific mAbs as probes. Autoantibodies to hsp70 also were detected in a minority of sera from patients with other rheumatic or viral diseases, but not in normal sera. These data may provide additional insight into etiologic and pathophysiologic mechanisms in this and related autoimmune disorders.

Autoantibodies↗
PubMed1988

Nature of IgG anti-lymphocyte autoantibody-reactive molecules shed from activated T cells in systemic lupus erythematosus.

Shedding of cell-surface antigens that react with anti-lymphocyte autoantibodies in systemic lupus erythematosus (SLE) is well-recognized, but the nature of such molecules is unknown. The present investigation demonstrates the rapid shedding of three IgG antibody target molecules of Mr 55,000, 37,000, and approximately 32,000 from the surface of mitogen-activated peripheral T cells during brief incubation at 37 degrees C. Sera lacking IgG anti-lymphocyte antibodies stained none of the three antigens. Absorption of antibody-positive sera with viable HSB-2 cells, a primitive T-cell line lacking HLA antigens and many CD antigens characteristic of mature peripheral T cells, eliminated staining of the shed molecules. These data delineate the number and estimated molecular mass of anti-lymphocyte autoantibody target molecules that are shed from the surface of T cells, and provide further insight into potential mechanisms by which anti-lymphocyte antibodies contribute to the pathogenesis of SLE and related disorders.

Autoantibodies↗
PubMed1987

Identification of three major target molecules of IgM antilymphocyte autoantibodies in systemic lupus erythematosus.

Three cell lymphocyte antigens of m.w. 55,000, 70,000, and 105,000 to 110,000 were identified by Western blotting as targets of IgM autoantibodies in serum from a group of 49 patients with systemic lupus erythematosus. The 55- and 70-kDa antigens were well expressed on unstimulated peripheral T cells, whereas the 105- to 110-kDa target was demonstrable only on mitogen-activated T cells and lymphoblastoid T cell lines. Localization of these molecules to the plasma membrane was established by cytoabsorption experiments in which IgM antibody staining of blotted antigens was specifically absorbed from systemic lupus erythematosus serum during 4 degrees C incubations with intact lymphocytes, and by their detection in purified lymphocyte plasma membranes. While the identity of these target antigens vis a vis known surface determinants was not defined, their expression on peripheral T cells from multiple donors and on cell lines of both undifferentiated (HSB-2) and phenotypically mature (Jurkat; HUT 78) types excluded alloantigens, major histocompatibility complex-encoded determinants, and most T cell differentiation antigens as candidates in this regard. Expression of the IgM autoantibody targets on HSB-2 cells argues against discrete T subset specificities as well. IgM reactivity with the 55-, 70-, and 105- to 110-kDa antigens by blotting was highly correlated with antilymphocyte antibody activity in complement-dependent cytotoxicity assays (Fisher's p less than 0.001), and paralleled flow microfluorimetric and microcytotoxicity quantitation of IgM antibody activity in serial observations of individual patients studied during different phases of disease activity. Taken together, these data suggest that IgM lymphocytotoxic antibodies in systemic lupus erythematosus are directed predominantly against a limited number of non-T cell subset-specific antigens.

Antibody Specificity↗
PubMed1987

IgG anti-lymphocyte antibodies in systemic lupus erythematosus react with surface molecules shared by peripheral T cells and a primitive T cell line.

IgG anti-T cell autoantibodies are common in SLE serum, react preferentially with activated lymphocytes, and exert early-phase inhibitory effects on antigen-induced T cell proliferation. Little is known about the target molecules in this system, however, because the low titer and low avidity of the most interesting antibodies limit their utility in conventional immunoprecipitation analyses. Therefore, Western blotting was used to demonstrate binding of IgG in anti-T cell antibody-positive SLE sera to four surface membrane molecules shared by peripheral T cells and HSB-2 cells. Molecules of Mr 90,000 and 55,000 were particularly reactive: each target was stained by IgG anti-lymphocyte antibodies in 11 patient sera (approximately 85%) in the panel. Targets of Mr 37,000 and 105,000 were encountered less frequently (six of 13 and one of 13 patients, respectively). It is unlikely that alloantibodies contributed to the staining patterns observed because reactivity with the four targets was consistently present when cell preparations from multiple unrelated donors were examined. The target molecules were localized to the plasma membrane by whole cell absorption/elution experiments, by the failure of chromatin (DNA/histone) to absorb antibodies to these antigens, and through the use of purified membranes as substrate for Western blotting. With the possible exception of the 105,000 Mr molecule, which is a major target in the IgM anti-T cell antibody system, evidence for the existence of neoantigens as a basis for increased reactivity of SLE IgG with activated T cells was not obtained. The identity of the IgG antibody-reactive molecules with respect to known T cell antigens was not determined, although evidence against the existence of antibodies to Tac (IL 2 receptor) and the transferrin receptor was obtained in monoclonal antibody pre-clearing experiments. Nonetheless, the observation that a limited number of major IgG autoantibody target antigens on activated peripheral T cells are shared by HSB-2 cells, a primitive T cell line expressing few of the differentiation antigens characteristic of mature T cells, should provide a basis for more definitive characterization of antigens in this system in the future.

Antibody Specificity↗
PubMed1987

Subset specificity of antilymhocyte antibodies in systemic lupus erythematosus. II. Preferential reactivity with T4 + cells is associated with relative depletion of autologous T4 + cells.

Using indirect immunofluorescence and flow cytometry, we determined the proportion and number of T3+, T4+, and T8+ cells in the peripheral blood of patients with systemic lupus erythematosus whose sera were positive for cold-reactive antilymphocyte antibodies versus values in patients whose sera were negative for these antibodies. There was a disproportionate reduction in T4+ peripheral lymphocytes when cold-reactive antilymphocyte antibodies preferentially cytotoxic for this subpopulation were present in autologous serum. The decrease in this subset was responsible for a reduction in the T4:T8 ratio; variation in the number and proportion of T8+ cells was insignificant. A similar, but autoantibody-independent, alteration in the T4+ subpopulation was found in patients who were receiving prednisone therapy. A relationship between T cell population abnormalities and systemic lupus erythematosus disease activity, per se, was not observed.

Antibody Specificity↗
PubMed1986

Modulation of IgM anti-lymphocyte antibody-reactive T cell surface antigens in systemic lupus erythematosus.

Cold-reactive lymphocytotoxic autoantibodies are present in the serum of most patients with active systemic lupus erythematosus (SLE) and may be important for the development of the lymphopenia and T cell dysfunction characteristic of this disorder. Neither the mechanisms of autoantibody action in this regard, nor the nature of the relevant T cell membrane target molecules have been defined, however. In the present investigation, preincubation of T cells with SLE serum at 37 degrees C reduced their reactivity with SLE IgM anti-lymphocyte autoantibodies, as demonstrated by indirect immunofluorescence and complement-dependent cytotoxicity. Modulation was restricted to SLE IgM autoantibody-reactive antigen; monoclonal antibody staining of various T cell differentiation and activation antigens remained unchanged. Loss of antigen from the surface membrane was rapid, but transient. A nadir was reached after approximately 120 min of 37 degrees C incubation, followed by essentially complete reexpression of antigen several hours later. Although modulation occurred spontaneously at 37 degrees C in the absence of SLE serum, loss of antigen was enhanced by IgM anti-lymphocyte autoantibodies, despite their low thermal amplitude. Modulation was inhibited by sodium azide, by fixation of cells with paraformaldehyde, and by low incubation temperatures. Colchicine and cytochalasin D had no effect on this process, suggesting that the integrity of the cytoskeleton was not essential. Cycloheximide did not prevent loss of antigen, but inhibited its reexpression. In experiments to determine the fate of modulated antigen, both intracytoplasmic accumulation and shedding from the cell surface were demonstrated. Only shedding was increased by the presence of anti-lymphocyte antibodies, however. These studies delineate modulation of T cell membrane antigen as a new mechanism for anti-lymphocyte autoantibody action in SLE. The occurrence of modulation at physiologic temperatures in vitro suggests that a similar phenomenon of potential relevance to T cell dysfunction may obtain in patients with this disorder.

Antigen-Antibody Reactions↗
PubMed1985

Surface antigen specificity of cold-reactive IgM antilymphocyte antibodies in systemic lupus erythematosus.

Monoclonal antibodies to known surface antigens on B cells and on resting and activated T cells of various types were used in several approaches to examine the specificity of IgM antilymphocyte antibodies in systemic lupus erythematosus (SLE). Surface determinants that were sought included: T3, T11, Leu-1, Leu-8 (pan-T); T4, T8 (T subset); beta 2-microglobulin (beta 2m); L243, Leu-10 (DR and DS/DC framework, respectively); anti-Tac (interleukin-2 receptor); 5E9 (transferrin receptor); and 4F2, AA1 (other activation antigens). The first strategy was based on inhibition of rosette formation between mouse monoclonal antibody-coated targets and anti-mouse IgG-coated erythrocytes by SLE sera, either directly at 4 degrees C or after modulation of IgM antilymphocyte antibody-reactive target cell antigen at 37 degrees C. Significant rosette inhibition, defined as greater than 2 standard deviations from the mean value for 10 control sera, was seen only for beta 2m (13 of 20 SLE sera were positive; inhibition = 15-58%). Next, relative fluorescence intensity of lymphocyte staining by monoclonal antibodies was assessed by flow microfluorometry after preincubation of cells with SLE serum at 4 degrees C or after modulation of SLE antibody-reactive antigen. Modulation markedly reduced or eliminated SLE antilymphocyte antibody IgM staining. Except for beta 2m, neither cold nor warm temperature preincubations altered the relative fluorescence intensity for the known surface antigens. These data confirm anti-beta 2m as a common antibody specificity in SLE and suggest that antilymphocyte antibodies in this disorder are not directed to Ia or to certain other defined lymphocyte antigens of functional interest.

Antibody Specificity↗
PubMed1985

Subset specificity of antilymphocyte antibodies in systemic lupus erythematosus. Preferential reactivity with cells bearing the T4 and autologous erythrocyte receptor phenotypes.

The relative specificity of systemic lupus erythematosus antilymphocyte antibodies for T cell subsets bearing the OKT4, OKT8, or autologous erythrocyte rosette (A-RFC) markers was examined in complement-dependent microcytotoxicity assays and by indirect immunofluorescence. Target cells included normal OKT4+ or OKT8+ T cell clones established from mitogen-activated blasts, resting or phytohemagglutinin-activated peripheral T cells highly enriched for OKT4+ cells or OKT8+ cells, and A-RFC+ and A-RFC- populations. In the majority of sera, cytotoxicity for T4+ cells was greater than that for T8+ cells regardless of cellular activation status. Overall cytotoxicity was considerably higher for activated cells, however, especially when warm assay temperatures were used. A-RFC+ targets were more reactive than nonrosetting T cells, and this was associated with strikingly higher relative fluorescence intensity of IgM staining. Despite these consistent differences in relative cytotoxicity or staining, antibody titers against all cell types were strongly correlated in individual sera. Absorption experiments failed to demonstrate distinct antibody specificities for T4+ and A-RFC+ cells. These data suggest that the major determinant of cytotoxic reactivity may be a single or limited number of surface antigens common to all T cells. Superimposed on this dominant system(s) is a special reactivity with certain distinct subsets and with activated T cells generally.

Antibody Specificity↗
PubMed1985

Rheumatology training at internal medicine and family practice residency programs.

The Medical Research Education Subcommittee of the American Rheumatism Association surveyed a random selection of large and small programs in internal medicine and family practice residency programs in order to evaluate their rheumatology training. Formal rheumatology training is offered in 90% of these residency programs, but many available positions are not being filled. A full-time staff rheumatologist was present at 69% of large internal medicine programs, 32% of small internal medicine programs, and 11% of family practice programs. The methods of rheumatology training are similar in most programs, although small internal medicine programs and family practice programs more often utilize physicians' offices or outside medical centers for the rheumatology elective training. A majority of the directors of these residency programs thought that many basic skills and techniques were not taught adequately and that the training of their rheumatology residents was not equal to that of residents in cardiology or gastroenterology.

Evaluation Studies as Topic↗
PubMed1985

Relationship of anti-beta 2-microglobulin antibodies to T11 and T-cell activation in systemic lupus erythematosus.

Monoclonal anti-beta 2-microglobulin (beta 2m) inhibited in a specific, dose-dependent fashion both in vitro tetanus toxoid-induced human-T-cell proliferation and sheep erythrocyte (E)-rosette formation, a function of the 50 kDa T11 molecule. In these respects, anti-beta 2m exhibited effects similar to those of sera from patients with SLE. Although 10 of 16 SLE sera contained antibody to beta 2m in monoclonal rosette inhibition assays, the presence of antibody of this specificity contributed only partially to the capacity of SLE serum to inhibit E-rosette formation or the T-cell response to tetanus toxoid. Removal of anti-beta 2m from SLE serum by solid phase absorption with beta 2m-Sepharose 4B reduced inhibition of the tetanus toxoid response and E-rosette formation in certain cases, but to a lesser extent than that observed following absorption with T-cell blasts, which completely eliminated inhibitory activity. Neither SLE antilymphocyte antibodies (including anti-beta 2m) nor heterologous anti-beta 2m were directed to the E receptor binding site (T11(1) epitope), as indicated by failure to inhibit OKT11 monoclonal antibody rosette formation or to reduce the relative intensity of OKT11 immunofluorescent staining. These data suggest an interesting functional relationship between beta 2m, the E receptor, and T-cell activation. While anti-beta 2m antibodies in SLE exert some inhibitory effect on antigen-induced T-cell proliferation, other distinct autoantibody systems to T-cell activation antigens appear to play the predominant role in this regard.

Antibodies↗
PubMed1985

Anti-lymphocyte antibodies in systemic lupus erythematosus.

Patients with systemic lupus erythematosus frequently develop antilymphocyte antibodies as measured by complement-dependent cytotoxicity and immunofluorescence assays. Highest titres of both of the major IgM and IgG classes occur during phases of active disease, and their presence is associated with essentially the entire spectrum of immune system functional abnormalities in this disorder. While the full range of antibody specificities requires further clarification, antibodies to many discrete lymphocyte populations have been described, including B cells, T cells, and T cell subsets. Antibodies to T cell subsets are of special interest because of their relationship with subset depletion in vivo, and their capacity to reproduce, through effects on normal cells in vitro, the same types of immunoregulatory abnormalities characteristic of lymphocytes isolated from patients with SLE. Suppressor/inducer and suppressor/effector T cells appear to be the main targets in this regard. Antibodies specific for activated T lymphocytes exist as well, and this type has the unusual property of interfering with events operant in production of/response to interleukin-2, a critical step controlling the expansion of specifically-reactive T cells and the induction of other lymphokines. In addition to complement-mediated lysis and antibody-dependent cell-mediated cytotoxicity, anti-lymphocyte antibodies have the potential to influence immune system function by several non-cytotoxic mechanisms, including surface antigen modulation and ligand/receptor triggering. Despite the large amount of data which has been accumulated concerning the cell type specificity and functional effects of anti-lymphocyte antibodies in SLE, little is known about the nature of the surface membrane molecules with which they react. Application of cell cloning and molecular biology technology should rectify this deficiency in the near future. Although it is likely that antilymphocyte antibodies are of relevance to immune system pathophysiology in SLE, it remains to be determined whether these interesting antibodies reflect secondary events, or have some more fundamental significance.

Antibody Specificity↗
PubMed1985

Disease-associated loss of erythrocyte complement receptors (CR1, C3b receptors) in patients with systemic lupus erythematosus and other diseases involving autoantibodies and/or complement activation.

Although surface membrane density of complement receptor type one (CR1) on erythrocytes (E) is probably an inherited trait among normal individuals, recent evidence from our laboratories suggests that the reduced number of CR1 per E observed in patients with systemic lupus erythematosus (SLE) results from acquired as well as genetic factors. In the present investigation, the number of CR1 per E was quantitated with 125I-monoclonal anti-CR1 and was found to vary inversely with disease activity in patients with SLE who were followed serially for as long as 14 mo. Although evidence for E surface-bound immune complexes or fixed C3b/iC3b was not obtained, periods of disease activity and low amounts of CR1 per E correlated with the presence of 100 to 800 molecules per E of fixed C3dg fragments (less than 100 C3dg per E in normal subjects). Reduced CR1 and excess fixed C3dg on E also were observed in patients with other disorders associated with complement activation, including chronic cold agglutinin disease, autoimmune hemolytic anemia, paroxysmal nocturnal hemoglobinuria (PNH), Sjögren's syndrome, and mycoplasma pneumonia. A significant negative correlation (r = -0.498) between CR1/E and fixed C3dg/E was demonstrable in 255 individual assays evaluated by regression analysis. CR1 decreased and fixed C3dg increased during active disease; the converse was obtained during remission. In patients with active SLE, both serum complement activity and E CR1 decreased, whereas fixed C3dg fragments increased. By piecewise linear regression analysis, the appearance of 100 to 400 C3dg molecules on patients' E corresponded to a 27 to 60%, reduction in the number of CR1 per E (p less than 0.0002), confirming that fixation of C3 to E was correlated with a loss of CR1. In patients with PNH, low values for CR1 were observed on moderately complement-sensitive PNH type II E in association with increased fixed C3 fragments; however, the markedly complement-sensitive PNH type III E had essentially normal amounts of CR1 and bore little fixed C3. The addition of soluble DNA/anti-DNA immune complexes to normal blood generated levels of fixed C3dg fragments on E comparable to those observed on E from patients with SLE. Kinetic experiments indicated that C3b was fixed to E during the process of immune complex binding and release from E CR1, and that this fixed C3b was subsequently degraded rapidly to fixed iC3b and more slowly to fixed C3dg without the loss of CR1 that occurs in vivo.(ABSTRACT TRUNCATED AT 400 WORDS)

Anemia, Hemolytic↗
PubMed1984

Inhibition of soluble antigen-induced T cell proliferation by warm-reactive antibodies to activated T cells in systemic lupus erythematosus.

One of the fundamental immunologic characteristics of systemic lupus erythematosus (SLE) is a depressed T cell proliferative response to various specific and nonspecific stimuli. Both intrinsic cellular defect(s) and inhibitory influences of humoral factors, e.g., antilymphocyte autoantibodies or immune complexes, have been postulated to underly this functional abnormality. Because patient serum can induce SLE-like T cell dysfunction in normal cells, an extrinsic mechanism is probably responsible, but the nature and site of action of this humoral activity has not been defined. This laboratory recently described a novel antibody specific for activated T cells in SLE, which raised the possibility that suppression of T cell proliferation by SLE serum involved antibodies directed to surface determinants expressed during the process of activation. In experiments to examine this concept further, relatively warm-reactive antibodies to T cell blasts were found to inhibit strongly the well-characterized T cell response to tetanus toxoid. These antibodies were distinct from conventional cold-reactive IgM antibodies to resting T cells, which exhibited little inhibitory activity. Inhibition involved noncytotoxic effects on early activation events at the level of the responding T cell, which markedly reduced the expression of receptors for interleukin 2. Inhibitory effects on antigen-pulsed macrophages or on T cells already committed to proliferate were not demonstrable. Anti-T blast antibodies were characteristic of active SLE and were detected only occasionally in patients with inactive disease or non-SLE rheumatic disorders. Although the exact antigenic specificity was not identified, considerable evidence was obtained against the presence of antibodies to Ia and certain other surface determinants of functional relevance. Our observations concerning the suppressive effects of anti-T blast antibodies in SLE serum on the T cell response to tetanus toxoid should provide new insight into mechanisms of in vivo T cell dysfunction in this and other immunologic disorders.

Antibodies, Monoclonal↗
PubMed1983

An evaluation of the annual meeting of the American Rheumatism Association. Results of a membership survey.

Members of the American Rheumatism Association (ARA) were surveyed to determine their views on the content and quality of their annual meeting. Responses were received from 1,208 members. ARA members were generally positive about the major components of the annual meeting program, but there were significant differences in opinion between practitioners and academicians. Practitioners favored a reduction in basic science material and an increase in didactic clinical sessions. Academicians were more likely to feel that recent annual meetings have adequately addressed their educational needs. These findings have implications for the planning of future annual meetings of the ARA.

Congresses as Topic↗
PubMed1983

Intrathecal IgG synthesis and blood-brain barrier impairment in patients with systemic lupus erythematosus and central nervous system dysfunction.

Paired serum and cerebrospinal fluid specimens from 19 patients with SLE and central nervous system dysfunction were studied with respect to cerebrospinal fluid IgG index (a measure of intrathecal IgG synthesis), isoelectric focusing using immunoperoxidase staining techniques to detect oligoclonal IgG, and determination of the cerebrospinal fluid/serum albumin quotient (Q albumin) as a measure of blood-brain barrier integrity. Twenty-five patients without neurologic disease and 70 patients with a variety of non-SLE neurologic disorders were also studied for comparison. Of most interest was the observation that 42 percent of the patients with SLE had cerebrospinal fluid oligoclonal IgG, usually in association with elevation of the cerebrospinal fluid IgG index. In addition, two of the cerebrospinal fluid specimens that exhibited oligoclonal IgG also had increased titers of alpha-interferon. Q albumin was normal (under 9.0) in 12 of 13 patients with SLE, who had seizure, psychosis, or cranial neuropathy as principal central nervous system manifestations (mean +/- SD = 5.3 +/- 2.4), but was significantly elevated (mean +/- SD = 27.4 +/- 18.8, p less than 0.001) in five of six patients with diffuse, major central nervous system injury, for example, encephalopathy with coma, transverse myelopathy, paraparesis. Blood-brain barrier impairment was not correlated either with presence of circulating immune complexes or with other clinical or serologic evidence for extra-central nervous system disease activity. Taken together, the data suggest that, within the limitations of the techniques used, impairment of the blood-brain barrier in SLE may be secondary to the central nervous system lesion, rather than a result of systemic immune complex injury. In addition, substantial evidence is provided for an ongoing humoral immune response within the central nervous system in this disorder, which, in certain patients, may be associated with the production of intrathecal alpha-interferon.

Albumins↗
PubMed1983

Cryoglobulinemia.

A large number of disease states are characterized by cryoglobulinemia. Quantification and immunochemical classification of cryoglobulins in serum provide information of diagnostic and pathophysiologic utility. Thus, type I cryoglobulins consist of a monoclonal immunoglobulin of a single class and are associated with lymphoproliferative disorders, such as multiple myeloma. Type II (mixed) cryoglobulins contain monoclonal IgM or rheumatoid factor and polyclonal IgG, and occur in patients with Waldenstrom's macroglobulinemia or chronic active hepatitis, for example. In type III cryoglobulins, both the IgM and rheumatoid factor and the IgG components are polyclonal. A large number of autoimmune or infectious diseases exhibit type III cryoglobulinemia. In certain well-studied situations, type II and type III cryoglobulins have been shown to contain antigen-antibody complexes directly involved in tissue injury in vivo, e.g., DNA and anti-DNA in systemic lupus erythematosus.

Cryoglobulinemia↗
PubMed1983

Characterization of warm-reactive IgG anti-lymphocyte antibodies in systemic lupus erythematosus. Relative specificity for mitogen-activated T cells and their soluble products.

In addition to previously described cold-reactive IgM anti-lymphocyte antibodies maximally cytotoxic for resting cells at 15 degrees C, sera from patients with systemic lupus erythematosus (SLE) were found to contain a new type of antibody preferentially reactive at physiologic temperatures with mitogen-activated lymphocytes. This antibody lacked specificity for unstimulated lymphocytes, and was shown to be of the IgG class both by indirect immunofluorescence and in immunochemical experiments. Certain SLE sera also contained IgG antibodies with the capacity to develop plaques with mitogen-activated T lymphocyte preparations used in a reverse hemolytic plaque assay, indicating reactivity with products released by activated cells. The elimination of the ability of SLE sera to develop plaques after absorption with viable mitogen-stimulated lymphocytes, but not with resting cells, suggested that these antibodies were directed toward activation "neoantigen(s)" shed from the cell surface membrane. Surface membrane phenotype analyses performed by using a variety of monoclonal antibody reagents indicated that the plaque-forming cells (PFC) detected with SLE sera were activated T lymphocytes not restricted to single OKT4+, OKT8+, or Ia antigen+ subpopulations. Essentially all PFC expressed transferrin receptors. The present data raise the possibility that certain of the interesting effects of anti-lymphocyte antibodies on immunologic function in SLE may be mediated by interactions of these new type(s) of antibodies with activated lymphocytes or their products, rather than through blocking or depletion effects on resting precursor cells.

Antibody-Dependent Cell Cytotoxicity↗