Tráfico leucocitario y trastorno inflamatorio

  1. Prieto Martín, A.
  2. Barbarroja Escudero, J.
  3. Gómez Lahoza, A.M.
  4. Monserrat Sanz, J.
Revista:
Medicine: Programa de Formación Médica Continuada Acreditado

ISSN: 0304-5412

Año de publicación: 2017

Serie: 12

Número: 24

Páginas: 1408-1417

Tipo: Artículo

DOI: 10.1016/J.MED.2016.12.010 DIALNET GOOGLE SCHOLAR

Otras publicaciones en: Medicine: Programa de Formación Médica Continuada Acreditado

Objetivos de desarrollo sostenible

Resumen

ResumenIntroducción Las células inmunes patrullan el organismo buscando agentes patógenos que estimularán la producción de mediadores y la extravasación leucocitaria. Inicio de la respuesta inflamatoria (RI) local Las células infectadas y las células centinela inician la RI. El endotelio se activa y se extravasan líquidos, moléculas solubles y leucocitos. Propagación de la RI Líquidos, moléculas y células drenan desde el foco infeccioso propagando la RI a los órganos linfoides secundarios (OLS), donde las células dendríticas presentarán los antígenos (Ag) a los linfocitos T, y los complejos Ag-complemento estimularán a los linfocitos B. Repercusión sistémica de la RI La linfa eferente transportará mediadores inflamatorios hacia la circulación sanguínea desencadenando la respuesta de fase aguda en bazo, hígado y médula ósea. Respuesta adaptativa en los OLS Los linfocitos Ag-específicos iniciarán la respuesta clonal contra el patógeno y se diferenciarán en células efectoras y memoria. Las células efectoras vuelven a la sangre y a los tejidos infectados donde forman agregados de células linfoides (granulomas y folículos linfoides ectópicos) y eliminan al patógeno. Respuesta clínica La producción aumentada de mediadores solubles de la RI da lugar a patologías. Estos mediadores de la extravasación leucocitaria son posibles dianas terapéuticas en el control de la RI.

Referencias bibliográficas

  • Grakoui A, Bromley SK, Sumen C, Davis MM, Shaw AS, Allen PM. The immunological synapse: a molecular machine controlling T cell activation. Science. 1999;285(5425):221-7.
  • Pober JS, Sessa WC. Evolving functions of endothelial cells in inflammation. Nat Rev Immunol. 2007;7(10):803-15.
  • Jamieson T, Clarke M, Steele CW, Samuel MS, Neumann J, Jung A. Inhibition of CXCR2 profoundly suppresses inflammation driven and spontaneous tumorigenesis. J Clin Invest. 2012;122(9):3127-44.
  • Han KH, Tangirala RK, Green SR, Quehenberger O. Chemokine receptor CCR2 expression and monocyte chemoattractant protein-1-mediated chemotaxis in human monocytes. A regulatory role for plasma LDL. Arterioscler Thromb Vasc Biol. 1998;18(12):1983-91.
  • Ley K. The role of selectins in inflammation and disease. Trends Mol Med. 2003;9(6):263-8.
  • Wang L, Fuster M, Sriramarao P, Esko JD. Endothelial heparan sulfate deficiency impairs L-selectin- and chemokine-mediated neutrophil trafficking during inflammatory responses. Nat Immu-nol. 2005;6(9):902-10.
  • Sompayrac LM. How the immune system works. 5th ed. Hoboken, NJ: Ed Willey-Blackwell; 2015.
  • Mogensen TH. Pathogen recognition and inflammatory signaling in in-nate immune defenses. Clin Microbiol Rev. 2009;22(2):240-73.
  • Malissen B, Tamoutounour S, Henri S. The origins and functions of dendritic cells and macrophages in the skin. Nat Rev Immunol. 2014;14(6): 417-28.
  • Bryant VL, Ma CS, Avery DT, Li Y, Good KL, Corcoran LM. Cytokine mediated regulation of human B cell differentiation into Ig secreting cells: predominant role of IL-21 produced by CXCR5+ T follicular helper cells. J Immunol. 2007;179(12):8180-90.
  • Lin RH, Mamula MJ, Hardin JA, Janeway CA Jr. Induction of autoreactive B cells allows priming of autoreactive T cells. J Exp Med. 1991;173(6):1433-9.
  • Deenick EK, Hasbold J, Hodgkin PD. Decision criteria for resolving isotype switching conflicts by B cells. Eur J Immunol. 2005;35(10): 2949-55.
  • Jovani M, Danese S. Vedolizumab for the treatment of IBD: a selective therapeutic approach targeting pathogenic D4E7 cells. Curr Drug Targets. 2013;14(12):1433-43.
  • Santamaria Babi LF, Pérez Soler MT, Hauser C, Blaser K. Skinhoming T cells in human cutaneous allergic inflammation. Immunol Res. 1995; 14(4):317-24.
  • Felix J, Lambert J, Roelens M, Maubec E, Guermouche H, Pages C, et al. Ipilimumab reshapes T cell memory subsets in melanoma patients with clinical response. Oncoimmunology. 2016;5(7):1136045.
  • Tokoyoda K, Zehentmeier S, Hegazy AN, Albrecht I, Grün JR, Löhning M, et al. Professional memory CD4+ T lymphocytes preferentially reside and rest in the bone marrow. Immunity. 2009;30(5):721-30.
  • Sato K, Honda SI, Shibuya A, Shibuya K. Improved protocol for the isolation of naïve follicular dendritic cells. Mol Immunol. 2016;78:140-5.
  • Saadeh D, Kurban M, Abbas O. Update on the role of plasmacytoid dendritic cells in inflammatory/autoimmune skin diseases. Exp Dermatol. 2016;25(6):415-21.
  • Xu J, Lee MH, Chakhtoura M, Green BL, Kotredes KP, Chain RW. STAT2 is required for tlr-induced murine dendritic cell activation and cross presentation. J Immunol. 2016;197(1):326-36.
  • Horiuchi T, Mitoma H, Harashima S, Tsukamoto H, Shimoda T. Transmembrane TNF-alpha: structure, function and interaction with anti-TNF agents. Rheumatology (Oxford). 2010;49(7):1215-28.
  • Black RA, Rauch CT, Kozlosky CJ, Peschon JJ, Slack JL, Wolfson MF. A metalloproteinase disintegrin that releases tumour-necrosis factor-alpha from cells. Nature. 1997;385(6618):729-33.
  • Polepalle T, Moogala S, Boggarapu S, Pesala DS, Palagi FB. Acute Phase Proteins and Their Role in Periodontitis: A Review. J Clin Diagn Res. 2015;9(11):ZE01-5.
  • Sun L, Ye RD. Serum amyloid A1: structure, function and gene polymorphism. Gene. 2016;583(1):48-57.
  • Martínez-Murillo P, Pramanik L, Sundling C, Hultenby K, Wretenberg P, Spångberg M. CD138 and CD31 double-positive cells comprise the functional antibody secreting plasma cell compartment in primate bone marrow. Front Immunol. 2016;7:242.
  • Chaudhry H, Zhou J, Zhong Y, Ali MM, McGuire F, Nagarkatti PS. Role of cytokines as a double-edged sword in sepsis. In Vivo. 2013;27(6): 669-84.
  • Comerford I, Harata-Lee Y, Bunting MD, Gregor C, Kara EE, McColl SR. A myriad of functions and complex regulation of the CCR7/CCL19/CCL21 chemokine axis in the adaptive immune system. Cytokine Growth Factor Rev. 2013;24(3):269-83.
  • Cañete JD, Celis R, Yeremenko N, Sanmartí R, van Duivenvoorde L, Ramírez J. Ectopic lymphoid neogenesis is strongly associated with activation of the IL-23 pathway in rheumatoid synovitis. Arthritis Res Ther. 2015;17:173.
  • Colombel JF, Sandborn WJ, Reinisch W, Mantzaris GJ, Kornbluth A, Rachmilewitz D. Infliximab, azathioprine, or combination therapy for Crohn’s disease. N Engl J Med. 2010;362(15):1383-95.
  • Wiens A, Correr CJ, Venson R, Otuki MF, Pontarolo R. A systematic review and meta-analysis of the efficacy and safety of adalimumab for treating rheumatoid arthritis. Rheumatol Int. 2010;30(8):1063-70.
  • Keystone EC, Genovese MC, Klareskog L, Hsia EC, Hall ST, Miranda PC. Golimumab, a human antibody to tumour necrosis factor {alpha} given by monthly subcutaneous injections, in active rheumatoid arthritis despite methotrexate therapy: the GO-FORWARD Study. Ann Rheum Dis. 2009;68(6):789-96.
  • Smolen J, Landewé RB, Mease P, Brzezicki J, Mason D, Luijtens K. Efficacy and safety of certolizumab pegol plus methotrexate in active rheumatoid arthritis: the RAPID 2 study. A randomised controlled trial. Ann Rheum Dis. 2009;68(6):797-804.
  • Van der Heijde D, Klareskog L, Rodríguez-Valverde V, Codreanu C, Bolosiu H, Melo-Gomes J. Comparison of etanercept and methotrexate, alone and combined, in the treatment of rheumatoid arthritis: two-year clinical and radiographic results from the TEMPO study, a double- blind, randomized trial. Arthritis Rheum. 2006;54(4):1063-74.
  • Levin AD, Wildenberg ME, van den Brink GR. Mechanism of action of anti-tnf therapy in inflammatory bowel disease. J Crohns Colitis. 2016; 10(8):989-97.
  • Nanda KS, Cheifetz AS, Moss AC. Impact of antibodies to infliximab on clinical outcomes and serum infliximab levels in patients with inflammatory bowel disease (IBD): a meta-analysis. Am J Gastroenterol. 2013; 108(1):40-7.
  • Rennard SI, Dale DC, Donohue JF, Kanniess F, Magnussen H, Sutherland ER. CXCR2 Antagonist MK-7123. A Phase 2 Proof-of-Concept Trial for Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med. 2015;191(9):1001-11.
  • Strader CR, Pearce CJ, Oberlies NH. Fingolimod (FTY720): a recently approved multiple sclerosis drug based on a fungal secondary metabolite. J Nat Prod. 2011;74(4):900-7.
  • Chun J, Brinkmann V. A mechanistically novel, first oral therapy for mul-tiple sclerosis: the development of fingolimod (FTY720, Gilenya). Discov Med. 2011;12(64):213-28
  • Provost V, Larose MC, Langlois A, Rola-Pleszczynski M, Flamand N, Laviolette M. CCL26/eotaxin-3 is more effective to induce the migration of eosinophils of asthmatics than CCL11/eotaxin-1 and CCL24/eotax-in-2. J Leukoc Biol. 2013;94(2):213-22.
  • Ramakrishnan L. Revisiting the role of the granuloma in tuberculosis. Nat Rev Immunol. 2012;12(5):352-66.
  • Gürcan HM, Keskin DB, Stern JN, Nitzberg MA, Shekhani H, Ahmed AR. A review of the current use of rituximab in autoimmune diseases. Int Immunopharmacol. 2009;9(1):10-25.
Fuente de los datos: Dialnet