Artículo

Estamos trabajando para incorporar este artículo al repositorio
Consulte el artículo en la página del editor
Consulte la política de Acceso Abierto del editor

Abstract:

In the non-obese diabetic (NOD) mouse, a spontaneous model of type 1 diabetes (T1D), recent evidence suggests that Schwann cells (Scs) and neurons surrounding insulin-producing β cells of the islets of Langerhans are destroyed before β cells. During normal perinatal development, macrophages (MΦ) are involved in phagocytosis of apoptotic neurons. Pertinently, MΦ are already present at birth in NOD pancreata. Their possible abnormal control of nerve phagocytosis, together with transient β-cell hyperactivity and lymphocyte anomalies, might conjointly participate in T1D pathogenesis.

Registro:

Documento: Artículo
Título:Is innervation an early target in autoimmune diabetes?
Autor:Saravia, F.; Homo-Delarche, F.
Filiación:Inst. de Biol. y Med. Experimental, Obligado 2490, 1428 Buenos Aires, Argentina
CNRS UMR 7059, Université Paris 7/D. Diderot, 2, place Jussieu, 75251 Paris Cedex 05, France
Palabras clave:autoantigen; chemokine; cytokine; glucose 6 phosphatase; glutamate decarboxylase; growth factor; isoenzyme; protein subunit; autoimmune disease; catalysis; cell differentiation; environmental factor; enzyme activity; genetic polymorphism; genetics; human; insulin dependent diabetes mellitus; lymphocyte; multigene family; nerve cell; nervous system; non insulin dependent diabetes mellitus; nonhuman; organogenesis; pancreas islet beta cell; protein expression; review
Año:2003
Volumen:24
Número:11
Página de inicio:574
Página de fin:579
DOI: http://dx.doi.org/10.1016/j.it.2003.09.010
Título revista:Trends in Immunology
Título revista abreviado:Trends Immunol.
ISSN:14714906
CODEN:TIRMA
CAS:glucose 6 phosphatase, 9001-39-2; glutamate decarboxylase, 9024-58-2
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_14714906_v24_n11_p574_Saravia

Referencias:

  • Rosmalen, J.G., Islet abnormalities in the pathogenesis of autoimmune diabetes (2002) Trends Endocrinol. Metab., 13, pp. 209-214
  • Winer, S., Autoimmune islet destruction in spontaneous type 1 diabetes is not β-cell exclusive (2003) Nat. Med., 9, pp. 198-205
  • Hamilton-Williams, E.E., Beta cell MHC class I is a late requirement for diabetes (2003) Proc. Natl. Acad. U. S. A., 100, pp. 6688-6693
  • Bonner-Weir, S., Orci, L., New perspectives on the microvasculature of the islets of Langerhans in the rat (1982) Diabetes, 31, pp. 883-889
  • Solimena, M., GAD, diabetes, and Stiff-Man syndrome: Some progress and more questions (1994) J. Endocrinol. Invest., 17, pp. 509-520
  • Atouf, F., Expression of neuronal traits in pancreatic β cells. Implication of neuron-restrictive silencing factor/repressor element silencing transcription factor, a neuron-restrictive silencer (1997) J. Biol. Chem., 272, pp. 1929-1934
  • Edlund, H., Pancreatic organogenesis - developmental mechanisms and implications for therapy (2002) Nat. Rev. Genet., 3, pp. 524-532
  • Winer, S., Type I diabetes and multiple sclerosis patients target islet plus central nervous system autoantigens; Nonimmunized nonobese diabetic mice can develop autoimmune encephalitis (2001) J. Immunol., 166, pp. 2831-2841
  • Winer, S., T cells of multiple sclerosis patients target a common environmental peptide that causes encephalitis in mice (2001) J. Immunol., 166, pp. 4751-4756
  • Salomon, B., Development of spontaneous autoimmune peripheral polyneuropathy in B7-2-deficient NOD mice (2001) J. Exp. Med., 194, pp. 677-684
  • Ichikawa, M., IgG subclass switching is associated with the severity of experimental autoimmune encephalomyelitis induced with myelin oligodendrocyte glycoprotein peptide in NOD mice (1999) Cell. Immunol., 191, pp. 97-104
  • Slavin, A., Induction of a multiple sclerosis-like disease in mice with an immunodominant epitope of myelin oligodendrocyte glycoprotein (1998) Autoimmunity, 28, pp. 109-120
  • Saravia, F.E., Increased astrocyte reactivity in the hippocampus of murine models of type 1 diabetes: The nonobese diabetic (NOD) and streptozotocin-treated mice (2002) Brain Res., 957, pp. 345-353
  • Aloisi, F., Regulation of T-cell responses by CNS antigen-presenting cells: Different roles for microglia and astrocytes (2000) Immunol. Today, 21, pp. 141-147
  • Fischer, H.G., Reichmann, G., Brain dendritic cells and macrophages/microglia in central nervous system inflammation (2001) J. Immunol., 166, pp. 2717-2726
  • Durant, S., Proapoptosis and antiapoptosis-related molecules during postnatal pancreas development in control and nonobese diabetic mice: Relationship with innervation (2003) Lab. Invest., 83, pp. 227-239
  • Honjin, H., The innervation of the pancreas of the mouse, with special reference to the structure of the peripheral extension of the vegetative nervous system (1956) J. Comp. Neurology, 104, pp. 331-371
  • Sorenson, R.L., Structural and functional considerations of GABA in islets of Langerhans. Beta-cells and nerves (1991) Diabetes, 40, pp. 1365-1374
  • Saravia-Fernandez, F., Localization of gamma-aminobutyric acid and glutamic acid decarboxylase in the pancreas of the nonobese diabetic mouse (1996) Endocrinology, 137, pp. 3497-3506
  • Boitard, C., Peripherin: An islet antigen that is cross-reactive with nonobese diabetic mouse class II gene products (1992) Proc. Natl. Acad. Sci. U. S. A., 89, pp. 172-176
  • Kaufman, D.L., Spontaneous loss of T-cell tolerance to glutamic acid decarboxylase in murine insulin-dependent diabetes (1993) Nature, 366, pp. 69-72
  • Tisch, R., Immune response to glutamic acid decarboxylase correlates with insulitis in non-obese diabetic mice (1993) Nature, 366, pp. 72-75
  • Mei, Q., Early, selective, and marked loss of sympathetic nerves from the islets of BioBreeder diabetic rats (2002) Diabetes, 51, pp. 2997-3002
  • Saikumar, P., Apoptosis: Definition, mechanisms, and relevance to disease (1999) Am. J. Med., 107, pp. 489-506
  • Charré, S., Abnormalities in dendritic cell and macrophage accumulation in the pancreas of nonobese diabetic mice during the early neonatal period (2002) Histol. Histopathol., 17, pp. 393-401
  • Chernousov, M.A., Carey, D.J., Schwann cell extracellular matrix molecules and their receptors (2000) Histol. Histopathol., 15, pp. 593-601
  • Lilje, O., Armati, P.J., The distribution and abundance of MHC and ICAM-1 on Schwann cells in vitro (1997) J. Neuroimmunol., 77, pp. 75-84
  • Kwa, M.S., Autoimmunoreactivity to Schwann cells in patients with inflammatory neuropathies (2003) Brain, 126, pp. 361-375
  • Kaufman, D.L., Murder mysteries in type 1 diabetes (2003) Nat. Med., 9, pp. 161-162
  • O'Brien, B.A., Phagocytosis of apoptotic cells by macrophages from NOD mice is reduced (2002) Diabetes, 51, pp. 2481-2488
  • Fadok, V.A., Phagocyte receptors for apoptotic cells: Recognition, uptake, and consequences (2001) J. Clin. Invest., 108, pp. 957-962
  • Cha, S., Abnormal organogenesis in salivary gland development may initiate adult onset of autoimmune exocrinopathy (2001) Exp. Clin. Immunogenet., 18, pp. 143-160
  • Esch, T.R., Taubman, M.A., Autoantibodies in salivary hypofunction in the NOD mouse (1998) Ann. N. Y. Acad. Sci., 842, pp. 221-228
  • Jansen, A., An immunohistochemical study on organized lymphoid cell infiltrates in fetal and neonatal pancreases. A comparison with similar infiltrates found in the pancreas of a diabetic infant (1993) Autoimmunity, 15, pp. 31-38
  • Delovitch, T.L., Singh, B., The nonobese diabetic mouse as a model of autoimmune diabetes: Immune dysregulation gets the NOD (1997) Immunity, 7, pp. 727-738
  • Hampe, C.S., Glutamate decarboxylase (GAD) autoantibody epitope shift during the first year of type 1 diabetes (1999) Horm. Metab. Res., 31, pp. 553-557
  • Undlien, D.E., Insulin gene region-encoded susceptibility to IDDM maps upstream of the insulin gene (1995) Diabetes, 44, pp. 620-625
  • Todd, J.A., Wicker, L.S., Genetic protection from the inflammatory disease type 1 diabetes in humans and animal models (2001) Immunity, 15, pp. 387-395
  • Naya, F.J., Diabetes, defective pancreatic morphogenesis, and abnormal enteroendocrine differentiation in BETA2/neuroD-deficient mice (1997) Genes Dev., 11, pp. 2323-2334
  • Lieberman, S.M., Identification of the {beta} cell antigen targeted by a prevalent population of pathogenic CD8+ T cells in autoimmune diabetes (2003) Proc. Natl. Acad. Sci. U. S. A., 100, pp. 8384-8388
  • Martin, C.C., Upstream stimulatory factor (USF) and neurogenic differentiation/β- cell E box transactivator 2 (NeuroD/BETA2) contribute to islet-specific glucose-6-phosphatase catalytic-subunit-related protein (IGRP) gene expression (2003) Biochem. J., 371, pp. 675-686
  • Pleau, J.M., Pancreatic hormones and glutamic acid decarboxylase (GAD) expression in the mouse thymus: A real-time PCR study (2001) Biochem. Biophys. Res. Com., 283, pp. 843-848

Citas:

---------- APA ----------
Saravia, F. & Homo-Delarche, F. (2003) . Is innervation an early target in autoimmune diabetes?. Trends in Immunology, 24(11), 574-579.
http://dx.doi.org/10.1016/j.it.2003.09.010
---------- CHICAGO ----------
Saravia, F., Homo-Delarche, F. "Is innervation an early target in autoimmune diabetes?" . Trends in Immunology 24, no. 11 (2003) : 574-579.
http://dx.doi.org/10.1016/j.it.2003.09.010
---------- MLA ----------
Saravia, F., Homo-Delarche, F. "Is innervation an early target in autoimmune diabetes?" . Trends in Immunology, vol. 24, no. 11, 2003, pp. 574-579.
http://dx.doi.org/10.1016/j.it.2003.09.010
---------- VANCOUVER ----------
Saravia, F., Homo-Delarche, F. Is innervation an early target in autoimmune diabetes?. Trends Immunol. 2003;24(11):574-579.
http://dx.doi.org/10.1016/j.it.2003.09.010