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1.
Lett Appl Microbiol ; 72(6): 750-756, 2021 Jun.
Article in English | MEDLINE | ID: mdl-33651401

ABSTRACT

Legionella species are the causative agent of Legionnaires' disease, a potentially fatal bacterial pneumonia. New regulations and standards have prioritized the development of water safety plans to minimize the growth and spread of Legionella species in buildings. To determine the presence and type of Legionella in a water system, microbiological culturing is the gold standard method. However, recently new methodologies have been developed that claim to be sensitive and specific for Legionella at the genus or L. pneumophila at the species level. Published and anecdotal reports suggest that one of these newer culture-based, enzyme-substrate methods, the IDEXX Legiolert test, may exhibit false positivity with other microbes common to water sources. We experimentally evaluated the IDEXX Legiolert method using these other waterborne bacteria including Elizabethkingia meningoseptica, Pseudomonas aeruginosa, Proteus mirabilis and Serratia marcescens at real-world environmental concentrations. We saw false-positive results for the Legiolert test with several of these organisms, at sample concentrations as low as 60 CFU per ml. False-positive Legionella results can trigger costly remediation and water-use restrictions, that may be implemented while waiting for additional, confirmatory microbiological testing that could, in this case, yield no L. pneumophila.


Subject(s)
Environmental Monitoring/methods , Legionella pneumophila/isolation & purification , Legionnaires' Disease/prevention & control , Cross Reactions , False Positive Reactions , Humans , Legionella pneumophila/classification , Legionnaires' Disease/microbiology , Water , Water Microbiology , Water Supply
2.
Proc Natl Acad Sci U S A ; 98(20): 11521-6, 2001 Sep 25.
Article in English | MEDLINE | ID: mdl-11562472

ABSTRACT

In 1986, Kärre and colleagues reported that natural killer (NK) cells rejected an MHC class I-deficient tumor cell line (RMA-S) but they did not reject the same cell line if it expressed MHC class I (RMA). Based on this observation, they proposed the concept that NK cells provide immune surveillance for "missing self," e.g., they eliminate cells that have lost class I MHC antigens. This seminal observation predicted the existence of inhibitory NK cell receptors for MHC class I. Here, we present evidence that NK cells are able to reject tumors expressing MHC class I if the tumor expresses a ligand for NKG2D. Mock-transfected RMA cells resulted in tumor formation. In contrast, when RMA cells were transfected with the retinoic acid early inducible gene-1 gamma or delta (RAE-1), ligands for the activating receptor NKG2D, the tumors were rejected. The tumor rejection was mediated by NK cells, and not by CD1-restricted NK1.1(+) T cells. No T cell-mediated immunological memory against the parental tumor was generated in the animals that had rejected the RAE-1 transfected tumors, which succumbed to rechallenge with the parental RMA tumor. Therefore, NK cells are able to reject a tumor expressing RAE-1 molecules, despite expression of self MHC class I on the tumor, demonstrating the potential for NK cells to participate in immunity against class I-bearing malignancies.


Subject(s)
Killer Cells, Natural/immunology , Major Histocompatibility Complex , Membrane Proteins/genetics , Animals , B-Lymphocytes/immunology , Female , Immunoglobulin Fc Fragments/immunology , Immunologic Memory , Lymphocyte Depletion , Lymphoma/genetics , Lymphoma/immunology , Membrane Proteins/immunology , Mice , Mice, Inbred C57BL , Recombinant Fusion Proteins/immunology , Transfection , Tumor Cells, Cultured
3.
J Immunol ; 165(12): 7215-23, 2000 Dec 15.
Article in English | MEDLINE | ID: mdl-11120854

ABSTRACT

Chemoattractants are thought to be the first mediators generated at sites of bacterial infection. We hypothesized that signaling through G protein-coupled chemoattractant receptors may stimulate cytokine production. To test this hypothesis, a human mast cell line (HMC-1) that normally expresses receptors for complement components C3a and C5a at low levels was stably transfected to express physiologic levels of fMLP receptors. We found that fMLP, but not C3a or C5a, induced macrophage inflammatory protein (MIP)-1ss (CCL4) and monocyte chemoattractant protein-1 (CCL2) mRNA and protein. Although fMLP stimulated both sustained Ca(2+) mobilization and phosphorylation of extracellular signal-regulated kinase (ERK), these responses to C3a or C5a were transient. However, transient expression of C3a receptors in HMC-1 cells rendered the cells responsive to C3a for sustained Ca(2+) mobilization and MIP-1ss production. The fMLP-induced chemokine production was blocked by pertussis toxin, PD98059, and cyclosporin A, which respectively inhibit G(i)alpha activation, mitgen-activated protein kinase kinase-mediated ERK phosphorylation, and calcineurin-mediated activation of NFAT. Furthermore, fMLP, but not C5a, stimulated NFAT activation in HMC-1 cells. These data indicate that chemoattractant receptors induce chemokine production in HMC-1 cells with a selectivity that depends on the level of receptor expression, the length of their signaling time, and the synergistic interaction of multiple signaling pathways, including extracellular signal-regulated kinase phosphorylation, sustained Ca(2+) mobilization and NFAT activation.


Subject(s)
Chemokines/biosynthesis , DNA-Binding Proteins/physiology , GTP-Binding Proteins/metabolism , Mast Cells/immunology , Mast Cells/metabolism , Membrane Proteins , Mitogen-Activated Protein Kinases/physiology , Nuclear Proteins , Transcription Factors/physiology , Antigens, CD/biosynthesis , Antigens, CD/genetics , Calcium/physiology , Calcium Signaling/genetics , Calcium Signaling/immunology , Chemokine CCL4 , Chemokines/genetics , DNA-Binding Proteins/metabolism , Extracellular Space/metabolism , Extracellular Space/physiology , GTP-Binding Proteins/physiology , Hemagglutinins/biosynthesis , Hemagglutinins/genetics , Humans , Macrophage Inflammatory Proteins/biosynthesis , Mast Cells/enzymology , Mitogen-Activated Protein Kinases/metabolism , N-Formylmethionine Leucyl-Phenylalanine/metabolism , N-Formylmethionine Leucyl-Phenylalanine/pharmacology , NFATC Transcription Factors , Phosphorylation , Protein Kinase C/physiology , RNA, Messenger/biosynthesis , Receptor, Anaphylatoxin C5a , Receptors, Complement/biosynthesis , Receptors, Complement/genetics , Receptors, Formyl Peptide , Receptors, Immunologic/biosynthesis , Receptors, Immunologic/genetics , Receptors, Peptide/biosynthesis , Receptors, Peptide/genetics , Transcription Factors/metabolism , Transfection , Tumor Cells, Cultured
4.
J Exp Med ; 186(2): 307-12, 1997 Jul 21.
Article in English | MEDLINE | ID: mdl-9221760

ABSTRACT

Chronic inflammatory autoimmune diseases such as multiple sclerosis, diabetes, and rheumatoid arthritis are caused by CD4(+) Th1 cells. Because Th2 cells antagonize Th1 cell functions in several ways, it is believed that immune deviation towards Th2 can prevent or cure autoimmune diseases. Experimental autoimmune encephalomyelitis (EAE) is a demyelinating disease used as a model for multiple sclerosis. Using an adoptive transfer system we assessed the role of Th1 and Th2 cells in EAE. In vitro generated Th1 and Th2 cells from myelin basic protein (MBP)-specific TCR transgenic mice were transferred into normal and immunodeficient mice. Th1 cells caused EAE in all recipients after a brief preclinical phase. Surprisingly, Th2 cells also caused EAE in RAG-1 KO mice and in alphabeta T cell-deficient mice, albeit after a longer preclinical phase. Normal or gammadelta T cell-deficient mice were resistant to EAE induced by Th2 cells. The histopathological features of this disease resembled those of an allergic process. In addition, disease induction by Th1 cells was not altered by coadmininstration of Th2 cells in any of the recipients. These findings indicate that MBP-specific Th2 cells have the potential to induce EAE and that the disease induced by previously activated Th1 cells cannot be prevented by normal lymphocytes nor by previously activated Th2 cells.


Subject(s)
Encephalomyelitis, Autoimmune, Experimental/etiology , Myelin Basic Protein/immunology , Th2 Cells/physiology , Animals , Immunocompromised Host , Mast Cells/physiology , Mice , Mice, Inbred C57BL , Neutrophils/physiology , Th1 Cells/physiology , Tumor Necrosis Factor-alpha/physiology
5.
Lab Invest ; 76(1): 11-23, 1997 Jan.
Article in English | MEDLINE | ID: mdl-9010446

ABSTRACT

During inflammation, T cells transmigrate from the bloodstream into perivascular tissues. As T cells transmigrate, they undergo a series of attachments to and detachments from the endothelium and then extravasate into the extracellular matrix (ECM). T cell migration into the ECM involves a number of mechanisms that influence cell-ECM interactions. The modulation of integrin expression and affinity are two such mechanisms in which cells can alter their ability to interact with other cells and ECM. We show in vitro that transmigrated T cells exhibit down-regulation of very late activation antigen-4 and leukocyte function-associated antigen-1 integrin surface expression and a decrease in binding to recombinant vascular cell adhesion molecule-1 and recombinant intercellular adhesion molecule-1. Also, transmigrated T cells displayed an increase in binding to collagens I and IV and fibronectin. Further, brain sections of experimental autoimmune encephalomyelitis mice demonstrated that as T cells migrated farther into the tissue, very late activation antigen-4 expression was lost while CD4 expression remained unchanged. The significance of these findings in the modulation of the inflammatory response is discussed.


Subject(s)
Cell Adhesion , Endothelium, Vascular/physiology , Extracellular Matrix/physiology , T-Lymphocytes/physiology , Animals , Brain/immunology , Brain/pathology , Cell Movement , Cells, Cultured , Collagen/physiology , Encephalomyelitis, Autoimmune, Experimental/immunology , Encephalomyelitis, Autoimmune, Experimental/pathology , Endothelium, Vascular/immunology , Fibronectins/physiology , Flow Cytometry , Integrin alpha4beta1 , Integrins/biosynthesis , Intercellular Adhesion Molecule-1/pharmacology , Interleukin-2/pharmacology , Lymphocyte Function-Associated Antigen-1/biosynthesis , Mice , Mice, Inbred Strains , Myelin Basic Protein/pharmacology , Peptide Fragments/pharmacology , Receptors, Lymphocyte Homing/biosynthesis , Receptors, Very Late Antigen/biosynthesis , Recombinant Proteins/pharmacology , T-Lymphocytes/drug effects , T-Lymphocytes/immunology , Up-Regulation , Vascular Cell Adhesion Molecule-1/pharmacology , Vascular Cell Adhesion Molecule-1/physiology
6.
Science ; 273(5283): 1864-7, 1996 Sep 27.
Article in English | MEDLINE | ID: mdl-8791592

ABSTRACT

The mechanism of CD40 ligand (CD40L)-mediated in vivo activation of CD4(+) T cells was examined by investigation of the development of experimental allergic encephalomyelitis (EAE) in CD40L-deficient mice that carried a transgenic T cell receptor specific for myelin basic protein. These mice failed to develop EAE after priming with antigen, and CD4(+) T cells remained quiescent and produced no interferon-gamma (IFN-gamma). T cells were primed to make IFN-gamma and induce EAE by providing these mice with B7.1(+) antigen-presenting cells (APCs). Thus, CD40L is required to induce costimulatory activity on APCs for in vivo activation of CD4(+) T cells to produce IFN-gamma and to evoke autoimmunity.


Subject(s)
Antigen-Presenting Cells/immunology , CD4-Positive T-Lymphocytes/immunology , Encephalomyelitis, Autoimmune, Experimental/immunology , Lymphocyte Activation , Membrane Glycoproteins/immunology , Animals , Antigens, CD/biosynthesis , B7-1 Antigen/biosynthesis , B7-1 Antigen/immunology , B7-2 Antigen , Brain/immunology , Brain/pathology , CD40 Ligand , Encephalomyelitis, Autoimmune, Experimental/pathology , Interferon-gamma/biosynthesis , Interleukin-4/biosynthesis , Membrane Glycoproteins/biosynthesis , Mice , Mice, Transgenic , Myelin Basic Protein/immunology , Receptors, Antigen, T-Cell/immunology , Spinal Cord/immunology , Spinal Cord/pathology , Up-Regulation
7.
Proc Natl Acad Sci U S A ; 93(1): 388-91, 1996 Jan 09.
Article in English | MEDLINE | ID: mdl-8552644

ABSTRACT

Orally administered antigens induce a state of immunologic hyporesponsiveness termed oral tolerance. Different mechanisms are involved in mediating oral tolerance depending on the dose fed. Low doses of antigen generate cytokine-secreting regulatory cells, whereas high doses induce anergy or deletion. We used mice transgenic for a T-cell receptor (TCR) derived from an encephalitogenic T-cell clone specific for the acetylated N-terminal peptide of myelin basic protein (MBP) Ac-1-11 plus I-Au to test whether a regulatory T cell could be generated from the same precursor cell as that of an encephalitogenic Th1 cell and whether the induction was dose dependent. The MBP TCR transgenic mice primarily have T cells of a precursor phenotype that produce interleukin 2 (IL-2) with little interferon gamma (IFN-gamma), IL-4, or transforming growth factor beta (TGF-beta). We fed transgenic animals a low-dose (1 mg x 5) or high-dose (25 mg x 1) regimen of mouse MBP and without further immunization spleen cells were tested for cytokine production. Low-dose feeding induced prominent secretion of IL-4, IL-10, and TGF-beta, whereas minimal secretion of these cytokines was observed with high-dose feeding. Little or no change was seen in proliferation or IL-2/IFN-gamma secretion in fed animals irrespective of the dose. To demonstrate in vivo functional activity of the cytokine-secreting cells generated by oral antigen, spleen cells from low-dose-fed animals were adoptively transferred into naive (PLJ x SJL)F1 mice that were then immunized for the development of experimental autoimmune encephalomyelitis (EAE). Marked suppression of EAE was observed when T cells were transferred from MBP-fed transgenic animals but not from animals that were not fed. In contrast to oral tolerization, s.c. immunization of transgenic animals with MBP in complete Freund's adjuvant induced IFN-gamma-secreting Th1 cells in vitro and experimental encephalomyelitis in vivo. Despite the large number of cells reactive to MBP in the transgenic animals, EAE was also suppressed by low-dose feeding of MBP prior to immunization. These results demonstrate that MBP-specific T cells can differentiate in vivo into encephalitogenic or regulatory T cells depending upon the context by which they are exposed to antigen.


Subject(s)
Encephalomyelitis, Autoimmune, Experimental/immunology , Myelin Basic Protein/genetics , Receptors, Antigen, T-Cell/physiology , Administration, Oral , Animals , Dose-Response Relationship, Immunologic , Immune Tolerance , Interferon-gamma/biosynthesis , Interleukin-10/biosynthesis , Interleukin-2/biosynthesis , Interleukin-4/biosynthesis , Lymphocyte Activation , Mice , Mice, Inbred C57BL , Mice, Transgenic , Myelin Basic Protein/administration & dosage , Transforming Growth Factor beta/biosynthesis
8.
Proc Natl Acad Sci U S A ; 92(2): 354-8, 1995 Jan 17.
Article in English | MEDLINE | ID: mdl-7530361

ABSTRACT

Although the clonal selection theory states that lymphocytes should bear only a single specificity of receptor, there is much evidence that some T cells, at least, bear two receptors. Here, we have used mice transgenic for genes encoding an autoreactive T-cell receptor (TCR) to examine the specificity of T cells bearing two functional TCRs. We find that T cells developing in mice that do not express the major histocompatibility complex (MHC) molecule recognized as self by the transgene-encoded TCR express both this TCR and a second TCR that is specific for the MHC molecules of the strain in which it arose. Thus, these T cells have two TCRs, each specific for a distinct antigen bound to a distinct MHC molecule. In contrast, when raised in mice bearing the MHC for which the receptor is specific, T cells develop that express the transgene-encoded TCR almost exclusively. Such mice are highly susceptible to autoimmune disease. Our data suggest that on most T cells bearing two TCRs, only one is specific for peptides bound to self-MHC molecules and, thus, that expression of two TCRs does not usually confer reactivity to two unrelated antigens.


Subject(s)
Autoimmunity/immunology , Major Histocompatibility Complex/immunology , Receptors, Antigen, T-Cell/immunology , T-Lymphocytes/immunology , Animals , Autoimmune Diseases/immunology , Autoimmunity/genetics , Clone Cells , Encephalomyelitis/immunology , Flow Cytometry , H-2 Antigens/genetics , H-2 Antigens/immunology , Lymphocyte Activation , Mice , Mice, Inbred C57BL , Mice, Transgenic , Myelin Basic Protein/immunology , Peptide Fragments/immunology , Receptors, Antigen, T-Cell/genetics , Selection, Genetic , Spleen/cytology , Spleen/immunology , Thymus Gland/cytology , Thymus Gland/immunology
9.
J Clin Invest ; 93(4): 1700-8, 1994 Apr.
Article in English | MEDLINE | ID: mdl-7512990

ABSTRACT

An adoptive transfer model of insulin-dependent diabetes mellitus (IDDM) in the nonobese diabetic mouse was used to examine the roles of alpha 4-integrin, vascular cell adhesion molecule 1 (VCAM-1); and intercellular adhesion molecule 1 (ICAM-1) in the pathogenesis of autoimmune diabetes. Antibodies specific for both alpha 4-integrin and one of its ligands, VCAM-1, were able to delay onset of diabetes and decrease the incidence of the disease in adoptive transfer studies. This blocking of disease was accompanied by a marked decrease in lymphocytic infiltration of the islets of Langerhans. Furthermore, these antibodies preferentially block entrance of CD4 T cells into the tissue. Antibodies specific for ICAM-1 had little effect on the onset or incidence of IDDM. Thus, we conclude that an alpha 4-integrin-VCAM-1 interaction is important in T cell entry into the islets of Langerhans and in the pathogenesis of IDDM. In addition, the cascade of events leading to T cell transit across endothelium may be different for CD4 and CD8 cells, and may differ depending on the endothelium involved. Our results support the more general conclusion that an alpha 4-integrin-VCAM-1 interaction may be crucial in allowing activated effector CD4T cells to leave the blood and enter tissue to clear infection.


Subject(s)
Cell Adhesion Molecules/physiology , Diabetes Mellitus, Type 1/etiology , Integrins/physiology , T-Lymphocytes/physiology , Animals , Antibodies, Monoclonal/immunology , CD4-CD8 Ratio , Cell Adhesion Molecules/analysis , Immunotherapy, Adoptive , Integrins/analysis , Intercellular Adhesion Molecule-1 , Islets of Langerhans/pathology , Mice , Mice, Inbred NOD , Receptors, Very Late Antigen/physiology , Spleen/immunology , T-Lymphocytes/chemistry , T-Lymphocytes/pathology , Vascular Cell Adhesion Molecule-1
10.
Ann Chir Plast Esthet ; 38(4): 457-61, 1993 Aug.
Article in French | MEDLINE | ID: mdl-8074439

ABSTRACT

The authors analyse the principal complications of healing of tracheotomy orifices and their causes. Apart from the poor quality of the skin scar, often large and irregular, several other anomalies of the deep layers under the scar may be responsible for various deformities: adherent, depressed scars or scars which move with deglutition. Surgical reconstruction of the various planes and filling of the dead spaces limit the inaesthetic and uncomfortable aspects of these scars. The use of platysma muscle flaps which are mobilised to reconstruct correct subcutaneous planes appears to be an optimal solution combined with other specific procedures of the cutaneous and visceral planes.


Subject(s)
Cicatrix/surgery , Surgical Flaps , Tracheotomy , Adolescent , Adult , Cicatrix/etiology , Esthetics , Female , Humans , Male , Middle Aged , Neck Muscles/surgery
11.
J Exp Med ; 177(1): 57-68, 1993 Jan 01.
Article in English | MEDLINE | ID: mdl-7678116

ABSTRACT

Cloned CD4 T cell lines that recognize the Ac1-16 peptide of myelin basic protein bound to I-Au were isolated and used to analyze the immunopathogenesis of experimental autoimmune encephalomyelitis (EAE). T helper type 1 (Th1) clones induced disease, while Th2 clones did not. Using variants of a single cloned Th1 line, the surface expression of alpha 4 integrins (very late antigen 4 [VLA-4]) was identified as a major pathogenic factor. Encephalitogenic clones and nonencephalitogenic variants differ by 10-fold in their level of surface expression of alpha 4 integrin and in their ability to bind to endothelial cells and recombinant vascular cell adhesion molecule 1 (VCAM-1). The alpha 4 integrin-high, disease-inducing cloned Th1 T cells enter brain parenchyma in abundance, while alpha 4 integrin-low, nonencephalitogenic Th1 cells do not. Moreover, antibodies to alpha 4 integrin, its ligand VCAM-1, and intercellular adhesion molecule 1 all influence the pathogenicity of this encephalitogenic clone in vivo. The importance of the expression of VLA-4 for encephalitogenicity is not unique to cloned T cell lines, as similar results were obtained using myelin basic protein-primed lymph node T cells. alpha 4 integrin levels did not affect antigen responsiveness or production of the Th1 cytokines interleukin 2, interferon gamma, and lymphotoxin/tumor necrosis factor beta; and antibodies against alpha 4 integrin did not block antigen recognition in vitro. Thus, we conclude that surface expression of alpha 4 integrin is important in CD4 T cell entry into brain parenchyma. A general conclusion of these studies is that alpha 4 integrins may be crucial in allowing activated effector T cells to leave blood and enter the brain and other tissues to clear infections.


Subject(s)
Brain/immunology , CD4-Positive T-Lymphocytes/immunology , Receptors, Very Late Antigen/physiology , Animals , Antibodies, Monoclonal/immunology , CD4-Positive T-Lymphocytes/physiology , Cell Adhesion Molecules/physiology , Cell Movement , Clone Cells , Encephalomyelitis, Autoimmune, Experimental/etiology , Intercellular Adhesion Molecule-1 , Mice , Mice, Inbred BALB C , Myelin Basic Protein/immunology , Receptors, Very Late Antigen/analysis , Vascular Cell Adhesion Molecule-1
12.
Ann Chir Plast Esthet ; 36(2): 167-8, 1991.
Article in French | MEDLINE | ID: mdl-1718207

ABSTRACT

Cutaneous expansion, especially in the lower limb, is sometimes complicated by the development of partial dehiscence of the surgical scar or a small area of necrosis over an angle of the prosthesis. The expander implant can be salvaged by closing the dehiscence with surgical adhesive film which allows continuation of expansion while preventing herniation of the prosthesis.


Subject(s)
Surgical Wound Dehiscence/therapy , Tissue Adhesives/therapeutic use , Tissue Expansion , Humans , Occlusive Dressings , Surgical Wound Dehiscence/etiology , Tissue Expansion/adverse effects
13.
Ann Chir Plast Esthet ; 36(1): 31-44, 1991.
Article in French | MEDLINE | ID: mdl-1712164

ABSTRACT

Based on an analysis of the anatomical and physical data reported in the literature, the authors describe their personal technique based on an experience of 100 pedicled inguinal flaps. The authors define the current indications for this flap in reconstructive hand surgery. The quality of pedicled inguinal flaps makes this procedure a technique of choice in the emergency treatment of wounds of the hand.


Subject(s)
Hand Injuries/surgery , Hand/surgery , Surgical Flaps , Adolescent , Adult , Aged , Aged, 80 and over , Child , Emergencies , Female , Follow-Up Studies , Groin , Hand Injuries/rehabilitation , Humans , Male , Middle Aged , Splints , Suture Techniques
14.
Ann Chir Main Memb Super ; 10(5): 430-5; discussion 436, 1991.
Article in French | MEDLINE | ID: mdl-1725711

ABSTRACT

The main drawbacks of the use of a groin pedicle flap in emergency surgery for hand injuries are the declivitous position of the upper limb with a tendency towards oedema and the difficulty of instituting early rehabilitation because of the fact that the injured hand is fixed to the abdomen. Based on an extensive experience of 76 emergency flaps out of more than 100 flaps performed over the last ten years, the authors describe their flap raising technique which allows the formation of a long, closed tube compatible with early rehabilitation and also allowing the possible use of splints.


Subject(s)
Emergencies , Groin , Hand Injuries/surgery , Surgical Flaps/methods , Follow-Up Studies , Hand Injuries/rehabilitation , Humans , Male , Splints , Surgical Flaps/standards , Time Factors
15.
Eur J Immunol ; 20(10): 2249-57, 1990 Oct.
Article in English | MEDLINE | ID: mdl-1978709

ABSTRACT

Different isoforms of CD45 are expressed on naive and memory CD4 T cells in the mouse, as revealed by an antibody to a set of isoforms of CD45 that utilize exon B, called CD45RB. Cloned TH1 and TH2 lines also differ for expression of isoforms detected by this antibody. Differential expression of CD45 isoforms correlates with different behavior of cell surface molecules involved in transmembrane signal transduction. On naive T cells, CD4, CD45 and the CD3/T cell receptor complex behave as independent entities. On memory T cells, these three molecules are stably associated on the T cell surface. Furthermore, on TH2 cells, which express intermediate levels of CD45RB, CD4 is stably associated with CD45 isoforms other than CD45RB, but this complex is not associated with the CD3/T cell receptor. These results lead us to propose that immunological memory in CD4 T cells consists of an altered structure of the T cell's specific signal transduction apparatus controlled by low-molecular weight CD45 isoforms. This altered receptor structure would allow the more sensitive triggering of the T cell characteristic of memory cells. The organization of multimolecular signal transduction systems may be a general means by which cells alter their physiological behavior, allowing the acquisition of new phenotypic characteristics.


Subject(s)
Antigens, CD/immunology , Immunologic Memory/immunology , T-Lymphocytes/immunology , Animals , Antibodies, Monoclonal/immunology , Antigens, Differentiation/immunology , Antigens, Differentiation, T-Lymphocyte/immunology , CD3 Complex , CD4 Antigens/immunology , CD4-Positive T-Lymphocytes/immunology , Cell Count , Female , Flow Cytometry , Histocompatibility Antigens/immunology , Leukocyte Common Antigens , Lymphocyte Activation/immunology , Male , Mice , Mice, Inbred AKR , Mice, Inbred BALB C , Receptors, Antigen, T-Cell/immunology
16.
Ann Chir Plast Esthet ; 35(1): 47-52, 1990.
Article in French | MEDLINE | ID: mdl-1693827

ABSTRACT

The hatchet flap, well known for the repair after skin resection of the nasal pyramid, is adapted, in a cutaneo-aponeurotic form, to the laterofacial region. The authors describe the principle of the technique which they illustrate by several clinical cases. Its simplicity, its harmonious adaptation and its reliability led them to consider that it has a place in the therapeutic arsenal for skin repair after resection of jugal and temporo-jugal lesions.


Subject(s)
Face/surgery , Surgical Flaps , Aged , Female , Humans , Male , Middle Aged , Skin Neoplasms/surgery , Surgery, Plastic
17.
Ann Chir Plast Esthet ; 35(1): 53-6, 1990.
Article in French | MEDLINE | ID: mdl-1693828

ABSTRACT

The authors recall the advantages of low transcartilage incision in rhinoplasty and, by means of several technical details, illustrate the value of this approach in submucosal dissection. They emphasise the anatomical clarity, safety and rapidity of the technique.


Subject(s)
Rhinoplasty/methods , Cartilage/surgery , Humans , Nose/surgery
18.
Ann Chir Plast Esthet ; 35(6): 453-8, 1990.
Article in French | MEDLINE | ID: mdl-1706158

ABSTRACT

Tuberous breast is a so-called mammary deformity which associates: deficient and contracted base, enlarged nipple-areolar complex, glandular herniation through the areola. The parenchyma is reduced, cylindrical, asymmetric, and frequently posted. Surgery reveals a basic glandular ring. The gland passes through this ring like a "glove's finger", revealing the herniation. All the cases are very different, but the surgical correction is common: concentric skin excision for areolar reduction. "V" vertical excision, allowing gland dissection. Via the skin wedge of the "V", extended dissection is carried out and half of the breast is denuded. The inferior mammary sulcus is released. The basal ring is cut and the posterior breast tissue is radially incised to expanding base, the parenchyma is stretched out. Correction of volume abnormalities: augmentation (implant), posterior reduction of symmetry. Correction of ptosis by skin redraping over the new mammary shape.


Subject(s)
Breast/abnormalities , Surgery, Plastic/methods , Breast/surgery , Female , Humans , Postoperative Period , Prostheses and Implants , Suture Techniques
19.
Ann Chir Plast Esthet ; 35(6): 496-7, 1990.
Article in French | MEDLINE | ID: mdl-1706165

ABSTRACT

The authors present a very simple and very comfortable splinting device for use after rhinoplasty. It consists of a splint made from malleable plastic which can be moulded by soaking in water at 60 degrees C, allowing perfect modelling to the shape of the nose. This splint is held in place by means of Velcro bands which offer remarkable flexibility of use.


Subject(s)
Rhinoplasty/instrumentation , Splints , Hot Temperature , Humans
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