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B Alarcon

Publications and source records attributed to B Alarcon.

At least 19 recordsLinked to original sources
PubMed2003

[Percutaneous transluminal angioplasty and severe limb ischaemia].

OBJECTIVES: To determine the outcome and the place of transluminal angioplasty (ATL) in the treatment of severe limb ischaemia. MATERIALS AND METHODS: Seventy two legs at stage III and IV of Fontaine's classification have been exclusively treated by endoluminal procedures. The success was valued both on the haemodynamic post-operative improvement of the run-off flow and on the clinical statut leading to the conservation at mid-term of a functional limb. Patency and survival rate had been valued by actuarial method. RESULTS: Seventy percent of the limbs were haemodynamically improved. For the global population, a 48% clinical success rate was obtained at 6 months but 30.5% of limbs were loss. Primary patency rate was respectively 79, 71 and 68% at 6, 12 and 24 month. The quality of the run-off arteries has been the most influential factor. CONCLUSION: Endoluminal treatment of chronic limb ischaemia had lead to a clinical improvement in 48% of cases. Multi-stages and distal atherosclerotic disease of this patients limits ATL indications which results depend of run-off quality.

Adult↗
PubMed2001

[Decompensation of lower limb arteritis after bone and joint surgery].

PURPOSE OF THE STUDY: Decompensation of lower limb arteritis after bone and joint surgery is an unusual finding compared with the large number of procedures performed in both emergency and controlled settings. There is however a functional and limb-threatening risk that must not be overlooked. MATERIAL AND METHODS: We report a series of 9 patients followed in our department over the last 3 years. Emergency surgery had been required in 6 patients after trauma and 3 had undergone a planned orthopedic procedure. All the patients had at least one vascular risk factor, and 7 of them had a cardiovascular history. The inaugural sign was a trophic disorder due to a grade IV decompensated arteritis in 8 patients, including 2 with nonunion. Delay to treatment ranged from 1 to 3 months. Acute embolic ischemia required emergency care in 1 patient. RESULTS: A revascularization procedure was performed on 6 limbs and was successful in 3. There were also 6 amputations, three initially, 1 after septic shock and 2 because revascularization was impossible. Three of the amputations were required after failed revascularization. Prosthesis wearing and walking was possible in only two amputated patients. Overall rate of successful salvage was 33% (3 successful revascularizations among 9 limbs). One of the nonunions healed after revascularization; the limb was amputated for the other one. One patient died from septicemia. DISCUSSION: Our series further illustrates the severity of decompensated arteritis after bone and joint surgery, emphasizing the importance of searching for cardiovascular risk factors and functional signs suggestive of a vascular disorder. Arterial duplex Doppler and if necessary arteriography of the lower limbs should be obtained in case of doubt. Two different situations can be distinguished depending on the predictable vascular risk and the localization of the planned bone reconstruction. If the patient has an asymptomatic proximal arteritis and bone and joint surgery is planned above the knee, a revascularization procedure would not appear necessary prior to bone surgery. In other cases, it may be more advisable to treat the arteritis before attempting bone surgery. For trauma victims, the osteosynthesis technique depends greatly on knowledge of the vascular risk.

Aged↗
PubMed1998

Altered functional responsiveness of thymocyte subsets from CD3delta-deficient mice to TCR-CD3 engagement.

CD3delta-deficient (delta degrees) mice are defective in alphabeta T cell development. Here we explore the capacity of TCR-CD3 signaling complexes expressed on delta degrees thymocytes to mediate the following functional outcomes in response to antibody cross-linking: (i) the transition from the CD4-CD8- to CD4+CD8+ stage, (ii) the transition from the CD4+CD8+ to CD4+CD8- or CD4-CD8+ stages and (iii) the induction of apoptosis. We provide evidence that CD3deltaepsilon complexes are dispensable for mediating the anti-CD3-mediated CD4-CD8- to CD4+CD8+ transition. On the other hand, CD3delta is critical at the CD4+CD8+ stage. We demonstrate that CD4+CD8+ thymocytes from delta degrees mice, unlike delta degrees CD4-CD8- thymocytes and wild-type CD4+CD8+ thymocytes, require prolonged or consecutive stimuli to elicit functional responses. Depending on the nature of the secondary stimulus, delta degrees thymocytes can be induced to undergo apoptosis or preferential maturation to the CD4-CD8+ stage. Taken together these results indicate that the signaling capacity of the TCR-CD3 complex is noticeably altered in the absence of CD3delta. The essential role of CD3delta at the CD4+CD8+ stage of development correlates with the onset of TCRalpha rearrangement, consistent with a critical structural and/or functional relationship between CD3delta and TCRalpha.

Animals↗
PubMed1997

Construction of retroviral vectors carrying human CD3 gamma cDNA and reconstitution of CD3 gamma expression and T cell receptor surface expression and function in a CD3 gamma-deficient mutant T cell line.

CD3 gamma, a subunit of the T cell receptor-CD3 (TCR/CD3) complex, helps to support surface TCR/CD3 expression and participates in signal transduction for gene induction after antigen recognition by T lymphocytes, and in TCR/CD3 down-modulation. Humans with primary immunodeficiencies caused by inherited mutations in the CD3 gamma gene or in the gene encoding epsilon CD3é, another subunit of TCR/CD3 complex, have been previously reported. To develop a gene therapy protocol for CD3-deficient patients, CD3 gamma cDNA was orientationally inserted into two retroviral vectors (LNCX and LXSN), which resulted in recombinant vectors LNCG and LGSN, respectively. Two vector producer cell lines Am12/LNCG and Am12/LGSN were established from packaging cells GP+envAm12. Their mean viral titers were 6.5 x 10(6) and 2.0 x 10(7) cfu/ml, respectively, as shown by an improved retroviral vector production and transduction method that increases titers around five-fold over conventional methods. The presence of helper virus in vector stocks was tested by marker rescue assay and found to be < 1 cfu/ml. Southern blot analysis showed that multiple copies of the vectors were present in the genome of high-titer producers and that both vectors could transfer CD3 gamma cDNA into the genome of 3T3 cells. The vectors were used to correct in vitro a CD3 gamma-deficient Jurkat mutant cell line lacking TCR/CD3 expression and termed JGN (for Jurkat gamma negative). Both vectors increased TCR/CD3 expression in JGN (normally 2% using WT31 monoclonal antibody) to 34% and 37%, respectively, in G418-selected 3-week bulk cultures. Two clones from transduced JGN cells termed JGN/LNCG13 and JGN/LNCG15, with high TCR/CD3 expression (88% and 79%, respectively), were selected for further analyses. First, CD3 gamma protein reconstitution was demonstrated by immunoprecipitation. Second, interleukin-2 production after TCR/CD3 engagement and TCR/CD3 down-modulation in response to phorbol myristate acetate were shown to be comparable to wild-type Jurkat cells. We conclude that LNCG and LGSN may be useful for gene therapy purposes.

DNA, Complementary↗
PubMed1997

CD3 delta deficiency arrests development of the alpha beta but not the gamma delta T cell lineage.

The CD3 complex found associated with the T cell receptor (TCR) is essential for signal transduction following TCR engagement. During T cell development, TCR-mediated signalling promotes the transition from one developmental stage to the next and controls whether a thymocyte undergoes positive or negative selection. The roles of particular CD3 components in these events remain unclear. Indeed, it is unknown whether they have specialized or overlapping roles. However, the multiplicity of CD3 components and their evolutionary conservation suggest that they serve distinct functions. Here the developmental requirement for the CD3 delta chain is analyzed by generating a mouse line specifically lacking this component (delta-/- mice). Strikingly, CD3 delta is shown to be differentially required during development. In particular, CD3 delta is not needed for steps in development mediated by pre-TCR or gamma delta TCR, but is required for further development of thymocytes expressing alpha beta TCR. Absence of CD3 delta specifically blocks the thymic selection processes that mediate the transition from the double-positive to single-positive stages of development.

Animals↗
PubMed1992

[Prognostic factors of femoropopliteal shunts. Retrospective study of a series of 52 shunts].

Between January 1986 and January 1991, 52 femoropopliteal shunts were carried out in 51 patients for lesions defined by the Ad Hoc Committee as grade III in 36 cases, grade II in 10 and grade I in 6. The shunt graft used was the internal saphenous vein in situ in 34 cases, inversed in 13 cases, and a PTFE prosthesis in 5 cases. The postoperative course included 12 complications and one death. At the end of the study, 10 shunts had thrombosed and 4 patients had required a major amputation. Actuarial analysis at 5 year follow up showed primary permeability of 56% and secondary permeability of 60%. Statistical analysis of secondary permeability as a function of the distal bed, an associated diabetes or the in situ or inversed venous shunt, failed to demonstrate any significant difference. These femoropopliteal venous shunts in critical ischemias reduced the incidence of major amputations, the proportion of limbs saved being higher than that for shunt permeability from the 6th postoperative month. Poor results were recorded for femoropopliteal shunts using prostheses.

Adult↗
PubMed1991

Requirements for cell surface expression of the human TCR/CD3 complex in non-T cells.

The T-cell antigen receptor (TCR) consists of a glycoprotein heterodimer (alpha/beta or gamma/delta) which is non-covalently associated with at least four or five invariant polypeptides (CD3 gamma, delta, epsilon, zeta and eta). In T-cell variants lacking TCR alpha, beta or zeta, it has been shown that incomplete TCR/CD3 complexes are retained within the cell. To examine requirements for cell surface expression of TCR/CD3, we transfected COS monkey kidney cells with cDNAs encoding TCR alpha, beta and CD3 gamma, delta, epsilon and zeta. We report that cell surface appearance of TCR/CD3 on COS cells requires coordinate expression of all six proteins. In the absence of the zeta chain, subcomplexes comprising from two to five chains were readily demonstrable in COS cells, but they failed to reach the cell surface or to acquire N-linked oligosaccharide side chains indicating failure to reach the medial Golgi. Pulse-chase metabolic labelling of transfected COS cells showed that three chains (CD3 gamma, CD3 epsilon, and zeta) were stable while three (TCR alpha, TCR beta and CD3 delta) were rapidly degraded. In two- and three-chain co-transfections specific intracellular subcomplexes were formed between TCR alpha and CD3 gamma, TCR alpha and CD3 delta, or TCR beta and CD3 epsilon. Binary subcomplexes having at least one stable chain (CD3 epsilon - TCR beta) were stable while one formed by two unstable chains (TCR alpha - CD3 delta) was still degraded. Assembly of the TCR/CD3 complex in COS cells thus appears centered around the metabolically stable CD3 gamma and CD3 epsilon proteins. Site-specific mutations of the negatively-charged transmembrane amino acid of residues of the CD3 chains to alanines served to either abolish (for TCR alpha - CD3 delta and TCR beta - CD3 epsilon) or diminish (for TCR alpha -CD3 gamma) these TCR-CD3 interactions. These mutations had no effect, however, on CD3-CD3 interactions or upon synthesis, metabolism, or intracellular distributions of the CD3 proteins. The transmembrane domains of CD3 gamma, delta, and epsilon thus appear to play a major role in associations of CD3 with TCR chains.

Animals↗
PubMed1990

Human T cell leukemia virus type I prevents cell surface expression of the T cell receptor through down-regulation of the CD3-gamma, -delta, -epsilon, and -zeta genes.

Infection and transformation by human T cell leukemia virus type I (HTLV-I) up-regulates expression of several inducible genes including those coding for cytokines involved in the proliferation of normal and leukemic T cells. We demonstrate that HTLV-I can also shut off expression of the CD3-gamma, delta, epsilon, and zeta genes that code for the constant elements of the TCR for Ag. In addition, the T cell-specific CD3-epsilon enhancer was found to be inactive in a HTLV-I-infected T cell clone. This HTLV-I-infected T cell clone (827-p19-II) that could be cultured in the absence of IL-2 lacked the CD3 proteins but did express the TCR-alpha and -beta proteins intracellularly. In the absence of the CD3-gamma, delta, epsilon, and zeta polypeptide chains the disulfide bridged TCR-alpha/beta heterodimer was not formed and the Ag receptor did not appear at the cell surface. These results allowed two major conclusions: first, HTLV-I infection has an effect on the T cell specific regulatory elements that coordinately regulate CD3-gamma, delta, epsilon, and zeta expression and second, the CD3-gamma, delta, epsilon, and zeta proteins are necessary for formation and routing the variable TCR-alpha/beta (or -gamma/delta) heterodimer to the human T cell surface.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1990

Assembly and function of the T cell antigen receptor. Requirement of either the lysine or arginine residues in the transmembrane region of the alpha chain.

The T cell receptor (TCR) for antigen consists, on the majority of peripheral lymphocytes, of an immunoglobulin-like, disulfide-linked heterodimeric glycoprotein: the alpha and beta chain. These proteins are noncovalently linked to at least four nonvariant proteins which comprise the CD3 complex: CD3 gamma, delta, epsilon, and zeta. Whereas the TCR alpha and beta proteins have positively charged residues in the transmembrane region, all the CD3 proteins have similarly placed negatively charged amino acid residues. It has been suggested that these basic and acidic amino acid residues may play an important role in TCR.CD3 complex assembly and/or function. In this paper, the structural and functional role of the lysine and arginine residues of the TCR alpha chain was addressed using oligonucleotide mediated site directed mutagenesis. The Arg256 and Lys261 residues of the TCR alpha cDNA of the HPB-ALL cell line were mutated to either Gly256 and/or Ile261. The altered cDNAs were transfected into a TCR alpha negative recipient mutant cell line of REX, clone 20A. Metabolic labeling of the T cell transfectants showed that mutation of either the Arg256 or Lys261 amino acid residues had no effect on the ability of the TCR alpha chain to form either a heterodimer with the TCR beta chain or a complex with the CD3 gamma, delta, and epsilon proteins. Consequently, the Arg256 to Gly256 and Lys261 to Ile261 mutations did not prevent the formation of a mature, functional TCR.CD3 complex on the cell surface as determined by immunofluorescence, cell surface radioiodination, and the ability of the transfectants to mobilize intracellular calcium after stimulation with a mitogenic anti-CD3 epsilon monoclonal antibody. In contrast, a mutant cDNA in which both the Arg256 and Lys261 residues were mutated to Gly256 and Ile261, respectively, failed to reconstitute the cell surface expression of the TCR.CD3 complex and, consequently, the ability to respond to mitogenic stimuli. In the absence of both the Arg256 and Lys261 residues, TCR alpha beta heterodimer formation was not observed. Cotransfection studies in COS cells showed that the failure of assembly of a heterodimer was likely due to an inability of the mutated TCR alpha chain to form a subcomplex with either the CD3 gamma, delta, epsilon, or zeta proteins.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Sequence↗
PubMed1990

Congenital T-cell receptor immunodeficiencies in man.

The T-cell receptor (TCR) for antigen is a complex consisting of at least seven polypeptides chains. Two chains form the clonotypic heterodimer, which determines antigen-specificity. The other five constitute the monomorphic CD3 components, which are thought to be involved in signal transduction. We have reported a familial defect in the surface expression of the TCR/CD3 complex on otherwise phenotypically normal T lymphocytes. As a consequence of the surface defect, an impaired T-lymphocyte activation through the TCR and CD3 complex by both antigens and mitogens is observed in this type of immunodeficiency (ID) for which we propose the name TCR ID. In contrast, normal proliferative responses were recorded to TCR-independent activation or proliferation signals (i.e: anti-CD2, phorbol esters and IL-2). We believe that other ID with similar clinical and immunological characteristics, described before the general availability of monoclonal antibodies, may have also been TCR ID. Severe and mild clinical phenotypes of the disease exist which correlate with differences in the levels of TCR surface expression and of T-cell function in vitro. The biochemical basis of the defect in one of the cases thus far studied is an impaired association of CD3-zeta chain with the other chains of the complex. This defect prevented the maturation and transport of the incomplete complex to the cell surface. Due to the multi-subunit nature of the TCR/CD3 complex it is possible that other biochemical defects in TCR assembly may also give rise to TCR ID. The description of mild as well as a severe phenotype in TCR ID points to a threshold effect of TCR/CD3 expression necessary for normal T cell function in vivo since mild TCR ID is clinically asymptomatic. In contrast, severe TCR ID behaves as a clinical SCID, with clear autoimmune features and profound lymphoid tissue depletion. TCR ID and other naturally occurring SCID variants may shed light on fundamental questions of the development, function and biochemistry of the in vivo immune system. Their study and characterization also opens the door to somatic gene therapy in this kind of disorder, which is an obvious goal in ID research.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1989

T-cell antigen receptor (TCR)-alpha/beta heterodimer formation is a prerequisite for association of CD3-zeta 2 into functionally competent TCR.CD3 complexes.

In order to study the relationship between assembly, surface expression, and signal transduction of the alpha/beta T-cell antigen receptor-CD3 complex (TCR.CD3), a series of T-cell mutants with a partial block in assembly of the complex was generated. By chemical mutagenesis, we produced somatic cell variants of the human T-leukemia cell line, HPB-ALL, which expressed low amounts of TCR.CD3 complexes on their surface. RNA and protein analyses demonstrated that most variants synthesized normal amounts of the individual members of the complex, i.e. TCR-alpha, TCR-beta, CD3-gamma, -delta, -epsilon, and -zeta. In these variants, less than 10% of the TCR.CD3 complexes inside the cell contained the CD3-zeta 2 homodimer due to an intrinsic deficiency in the formation of the TCR-alpha/beta heterodimer. The low level of assembly of CD3-zeta 2 into the TCR.CD3 complex and an additional decrease in the rate of export of the TCR.CD3 complex from the endoplasmic reticulum explained the low level of expression of alpha/beta receptors on the surface of these mutants. Only cells with the complete set of subunits of the TCR.CD3 complex on their surface were capable of transducing CD3-mediated signals. The results presented in this paper indicate that TCR-alpha/beta heterodimer formation is an obligatory requirement for assemblage of CD3-zeta 2 into a functionally competent TCR.CD3 complex.

Antigens, CD↗
PubMed1989

Introduction of T cell receptor (TCR)-alpha cDNA has differential effects on TCR-gamma delta/CD3 expression by PEER and Lyon-1 cells.

A TCR heterodimer composed of a TCR gamma-chain and a TCR delta-chain was found to be expressed in association with CD3 by a small population of human peripheral blood T cells, thymocytes, and certain leukemic T cell lines. The leukemic T cell lines PEER and Lyon-1 express such a TCR-gamma delta/CD3 complex at the cell surface. In addition, PEER and Lyon-1 cells transcribe a productively rearranged TCR-beta gene. Introduction of TCR alpha-chain cDNA of human or murine origin resulted in cell surface expression of a TCR-alpha beta/CD3 complex on PEER and Lyon-1 cells. The expression of the TCR-gamma delta/CD3 complex on PEER cells was not affected by introduction of TCR-alpha cDNA. In contrast, introduction of a TCR-alpha cDNA and expression of the TCR-alpha beta/CD3 complex in Lyon-1 cells resulted in the disappearance of the TCR-gamma delta/CD3 complex. These data were confirmed by indirect immunofluorescence, at the protein level and by gene expression analysis. Triggering of the TCR-alpha beta/CD3 complexes by anti-CD3 mAb or anti-TCR mAb resulted in increased internal Ca2+ levels, indicating that these receptors were functional in signal transduction. These results indicate that, besides TCR gene rearrangements, membrane expression of TCR-alpha beta heterodimers may be important in regulating TCR-gamma delta cell surface expression.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1988

Transfection of genes encoding the T cell receptor-associated CD3 complex into COS cells results in assembly of the macromolecular structure.

The T cell antigen receptor (TCR) consists of a disulfide-linked TCR-alpha/beta heterodimer that is both structurally and functionally associated with a set of four non-covalently linked membrane proteins termed CD3-gamma, -delta, -epsilon, and -zeta. An additional protein described recently, CD3-omega, has been suggested to play a role in assembly of the CD3 complex on the basis of its transient association with the CD3 proteins early during biosynthesis. Association of all the proteins seems to be a prerequisite for intracellular transport, since mutants lacking either the TCR-alpha or -beta protein do not express the CD3 complex on the cell surface. CD3-cDNAs were transfected into COS cells in order to study the protein-protein interactions ruling the assembly of the CD3 macromolecular structure. CD3-delta-epsilon, CD3-gamma-epsilon, and CD3-gamma-delta-epsilon intermediates could be detected. These data indicated that a CD3 core structure could be formed in the absence of the other members of the complex (CD3-zeta, -omega, TCR-alpha, and -beta). Both the individual CD3 chains and the assembled CD3.gamma.delta.epsilon complexes could not be detected on the cellular surface but in an intracellular compartment, probably the endoplasmic reticulum or the cis Golgi. The transfection experiments allowed us to identify the 25-kDa member of the murine CD3 complex as CD3-epsilon m. Furthermore, a 23-kDa glycoprotein seen upon metabolic labeling of human T cells was shown to be an immature form of the CD3-gamma h protein.

Animals↗
PubMed1988

Abnormal T cells from MRL/Mp-lpr/lpr mice do not respond to anti-T-cell-receptor antibody or tumor promoter and calcium ionophore A23187 despite the presence of the T-cell-receptor complex and protein kinase c.

Abnormal T cells from autoimmune MRL/Mp-lpr/lpr mice express T-cell-receptor complexes on their surfaces. These receptors are nonfunctional, since monoclonal anti-T-cell-receptor antibody-conjugated beads, which normally activate receptor-bearing T cells, were unable to activate these abnormal T cells. In addition, these abnormal T cells are unresponsive to the synergistic effect of phorbolmyristate acetate (PMA) and calcium ionophore A23187, as quantitated by proliferation, interleukin-2(IL-2) production, and the expression of IL-2 receptors. The failure of abnormal T cells to respond to PMA is not due to the absence of PMA receptors since Scatchard plot analysis reveals that there are 1-1.5 X 10(5) PMA-binding sites/cell with a Kd of 6-10 nM on these abnormal T cells. Similar to normal T lymphocytes, protein kinase c activity can be readily detected in the cytosolic fraction of these abnormal T cells. More importantly, in vitro culture of the abnormal T cells with PMA results in translocation of protein kinase c activity from the cytosolic fraction to the membrane fraction. From these experiments we concluded that the defect in the signal-transducing machinery in MRL/Mp-lpr/lpr T cells is not due to the lack of PMA receptors or the absence of protein kinase c activity, but may result from events which occur after the activation and translocation of protein kinase c. However, whether defects in response to a physiological stimulus (i.e., anti-receptor antibody) could occur in a step prior to protein kinase c activation remains to be determined.

Animals↗
PubMed1988

Assembly of the human T cell receptor-CD3 complex takes place in the endoplasmic reticulum and involves intermediary complexes between the CD3-gamma.delta.epsilon core and single T cell receptor alpha or beta chains.

Functionally mature human T lymphocytes express a cell-surface receptor for antigen (T cell receptor (TCR)-CD3) composed of at least six polypeptides (TCR-alpha and -beta; T3-gamma, -delta, -epsilon, and -zeta). Immature thymocytes and variants of T cell lines lacking one of the TCR.CD3 polypeptide chains fail to express surface receptor and accumulate the other chains intracellularly. Here we show that the assembly of the TCR.CD3 complex within the endoplasmic reticulum (ER) began with a core of CD3-gamma, -delta, and -epsilon to which TCR-alpha and -beta bound. A recently described intracellular protein, CD3-omega, participated in the assembly since it was found to be associated with the free TCR-alpha or -beta chains or with the CD3 chains. CD3-omega dissociated as TCR.CD3 complexes were formed in the ER. Association of non-disulfide-linked TCR-alpha and -beta chains with CD3 was detected before that of disulfide-bridged TCR-alpha/beta heterodimers. These data suggest that during assembly, the association of TCR-alpha and -beta chains with the CD3 complex precedes the formation of a TCR-alpha/beta dimer. The existence of intermediates consisting of CD3-gamma, -delta, and -epsilon chains and a single TCR-alpha or -beta chain was also confirmed by using a series of variant T cell lines lacking the TCR-beta or -alpha chain, respectively. Once the single TCR-alpha and -beta chains were associated with CD3, disulfide linkages were formed, and a 70-kDa form of the TCR was detected within the ER. This intracellular precursor of the TCR.CD3 complex was subsequently processed into the mature 90-kDa TCR as the TCR.CD3 complex passed through the Golgi apparatus. Assembly of the TCR.CD3 complex is a rather rapid process, whereas export from the ER occurs at a slow rate. After 1 h, 75% of the receptor complex remained within the ER.

Cell Line↗
PubMed1987

T3-p28 is a protein associated with the delta and epsilon chains of the T cell receptor-T3 antigen complex during biosynthesis.

The human T cell receptor-T3 antigen complex is composed of at least five polypeptide chains. In addition to the 45-kDa/50-kDa heterodimer (alpha and beta chains) of the T cell receptor, the complex includes 25-kDa (T3-gamma) and 20-kDa (T3-delta) glycoproteins and a nonglycosylated 20-kDa (T3-epsilon) protein. Here we report that in pulse-chase biosynthetic labeling experiments we detect a new polypeptide chain (T3-p28) which is associated with the T3-delta and T3-epsilon chains during biosynthesis but not on the cell surface. T3-p28, which is not recognized by anti-T3 antibodies, can be chemically distinguished from the previously described T3-gamma chain. The carboxylic ionophore monensin blocks the apparent dissociation of T3-p28 from the T3-delta and T3-epsilon chains. Peripheral blood lymphocytes as well as all T cell leukemic lines tested contain T3-p28, except one HPB-ALL subline. Since the T3-p28 protein is only observed early in biosynthesis of T3-delta and T3-epsilon, it may function in intracellular transport or assembly of the T cell receptor-T3 complex.

Antigens, Surface↗