2008, Número 1
<< Anterior Siguiente >>
Rev Inst Nal Enf Resp Mex 2008; 21 (1)
Receptores de células NK (KIR): Estructura, función y relevancia en la susceptibilidad de enfermedades
Torres-García D, Barquera R, Zúñiga J
Idioma: Español
Referencias bibliográficas: 38
Paginas: 57-65
Archivo PDF: 95.79 Kb.
RESUMEN
Los receptores tipo inmunoglobulina de las células NK (en inglés,
Killer Immunoglobulin-like Receptor, KIR) son un conjunto de proteínas de superficie cuyos ligandos principales son moléculas de clase I del complejo principal de histocompatibilidad (en inglés,
Major Histocompatibility Complex, MHC). La actividad efectora de las células NK, está regulada por el balance entre señales de activación y de inhibición como resultado de la expresión de moléculas KIR con diferentes propiedades funcionales y de los genotipos HLA. La interacción KIR con sus ligantes HLA de clase I es de particular importancia en el control de las infecciones virales y del cáncer. Numerosos estudios han demostrado la importancia de las combinaciones KIR-HLA en la susceptibilidad y resistencia a enfermedades de etiología infecciosa, autoinmune y cáncer. El ejemplo más claro es la asociación de los genotipos homocigotos KIR2DL3/2DL3 y HLA-C1/C1 en el control de la infección por virus de hepatitis C. El estudio de los genotipos KIR, en el contexto de las enfermedades pulmonares, es un campo fértil ya que existe poco o nada de información en él, que potencialmente sería importante para la generación de nuevas líneas de investigación. Para ello, se debe seguir un estudio interdisciplinario acerca de la función de los dos juegos de moléculas del hospedero en la fisiología, tanto en condiciones de salud como de enfermedad, y el origen evolutivo de estas interacciones.
REFERENCIAS (EN ESTE ARTÍCULO)
Karimi M, Cao TM, Baker JA, Verneris RM, Soares L, Negrin RS. Silencing human NKG2D, DAP10, and DAP12 reduces cytotoxicity of activated CD8+ T cells and NK cells. J Immunol 2005;175:7819-7828.
Kelley J, Walter L, Trowsdale J. Comparative genomics of natural killer cell receptor gene clusters. PLoS Genetics 2005;1:129-139.
O’Connor GM, Hart OM, Gardiner CM. Putting the natural killer cell in its place. Immunology 2006;117:1-10.
Parham P. MHC class I molecules and KIRs in human history, health and survival. Nat Rev Immunol 2005;5:201-214.
Rajagopalan S, Long EO. Understanding how combinations of HLA and KIR genes influence disease. J Exp Med 2005;201:1025-1029.
Yawata M, Yawata N, Draghi M, Little AM, Partheniou F, Parham P. Roles for HLA and KIR polymorphisms in natural killer cell repertoire selection and modulation of effector function. J Exp Med 2006;203:633-645.
Carrington M, Norman P. The KIR gene cluster. 2003. The online books page. Acceso: http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mono_003.chapter.1.
Single RM, Martin MP, Gao X, et al. Global diversity and evidence for coevolution of KIR and HLA. Nat Genet 2007;39:1114-1119.
Moretta L, Moretta A. Killer immunoglobulin-like receptors. Curr Opin Immunol 2004;16:626-633.
Hey J. On the number of New World founders: a population genetic portrait of the peopling of the Americas. PLoS Biol 2005;3:e193.
Pavlova Y, Kolesar L, Striz I, Jabor A, Slavcev A. Distribution of KIR genes in the Czech population. Int J Immunogenet 2008;35:57-61.
Saxena RK. Ontogeny of inhibitory receptors for MHC molecules on NK cells. Immunol Today 1997;18:146.
Borrego F. The first molecular basis of the "missing self" hypothesis. J Immunol 2006;177:5759-5760.
Storkus WJ, Alexander J, Payne JA, Cresswell P, Dawson JR. The alpha 1/alpha 2 domains of class I HLA molecules confer resistance to natural killing. J Immunol 1989;143:3853-3857.
Saxena RK. Missing self by heterogeneous natural killer cells. J Biosci 1997;22:3-12.
Biassoni R, Falco M, Cambiaggi A, et al. Amino acid substitutions can influence the natural killer (NK)-mediated recognition of HLA-C molecules. Role of serine-77 and lysine-80 in the target cell protection from lysis mediated by "group 2" or "group 1" NK clones. J Exp Med 1995;182:605-609.
Colonna M, Spies T, Strominger JL, et al. Alloantigen recognition by two human natural killer cell clones is associated with HLA-C or a closely linked gene. Proc Natl Acad Sci USA 1992;89:7983-7985.
Winter CC, Long EO. A single amino acid in the p58 killer cell inhibitory receptor controls the ability of natural killer cells to discriminate between the two groups of HLA-C allotypes. J Immunol 1997;158:4026-4028.
Carr WH, Pando MJ, Parham P. KIR3DL1 polymorphisms that affect NK cell inhibition by HLA-Bw4 ligand. J Immunol 2005;175:5222-5229.
Vilches C, Parham P. KIR: diverse, rapidly evolving receptors of innate and adaptive immunity. Annu Rev Immunol 2002;20:217-251.
Khakoo SI, Carrington M. KIR and disease: a model system or system of models? Immunol Rev 2006;214:186-201.
Williams AP, Bateman AR, Khakoo SI. Hanging in the balance. KIR and their role in disease. Mol Interv 2005;5:226-240.
Shilling HG, Young N, Guethlein LA, et al. Genetic control of human NK cell repertoire. J Immunol 2002;169:239-247.
Nelson GW, Martin MP, Gladman D, Wade J, Trowsdale J, Carrington M. Cutting edge: heterozygote advantage in autoimmune disease: hierarchy of protection/susceptibility conferred by HLA and killer Ig-like receptor combinations in psoriatic arthritis. J Immunol 2004;173:4273-4276.
Martin MP, Gao X, Lee JH, et al. Epistatic interaction between KIR3DS1 and HLA-B delays the progression to AIDS. Nat Genet 2002;31:429-434.
Khakoo SI, Thio CL, Martin MP, et al. HLA and NK cell inhibitory receptor genes in resolving hepatitis C virus infection. Science 2004;305:872-874.
Romero V, Azocar J, Zúñiga J, et al. Interaction of NK inhibitory receptor genes with HLA-C and MHC class II alleles in Hepatitis C virus infection outcome. Mol Immunol 2008. En prensa.
Nelson GW, Martin MP, Gladman D, Wade J, Trowsdale J, Carrington M. Cutting edge: heterozygote advantage in autoimmune disease: hierarchy of protection/susceptibility conferred by HLA and killer Ig-like receptor combinations in psoriatic arthritis. J Immunol 2004;173:4273-4276.
Van der Slik AR, Koeleman BP, Verduijn W, Bruining GJ, Roep BO, Giphart MJ. KIR in type 1 diabetes: disparate distribution of activating and inhibitory natural killer cell receptors in patients versus HLA-matched control subjects. Diabetes 2003;52:2639-2642.
Zúñiga J, Romero V, Azocar J, et al. Interaction of KIR genes and G1M immunoglobulin allotypes confer susceptibility to type 2 diabetes in Puerto Rican Americans. Hum Immunol 2006;67:907-914.
uszczek W, Mañczak M, Cis³o M, et al. Gene for the activating natural killer cell receptor, KIR2DS1, is associated with susceptibility to psoriasis vulgaris. Hum Immunol 2004;65:758-766.
Naumova E, Mihaylova A, Stoitchkov K, Ivanova M, Quin L, Toneva M. Genetic polymorphism of NK receptors and their ligands in melanoma patients: prevalence of inhibitory over activating signals. Cancer Immunol Immunother 2005;54:172-178.
Hiby SE, Walker JJ, O’shaughnessy KM, et al. Combinations of maternal KIR and fetal HLA-C genes influence the risk of preeclampsia and reproductive success. J Exp Med 2004;200:957-965.
Ruggeri L, Capanni M, Urbani E, et al. Effectiveness of donor natural killer cell alloreactivity in mismatched hematopoietic transplants. Science 2002: 295:2097-2100.
Gagne K, Brizard G, Gueglio B, et al. Relevance of KIR gene polymorphisms in bone marrow transplantation outcome. Hum Immunol 2002:63:271-280.
Davies SM, Ruggieri L, DeFor T, et al. Evaluation of KIR ligand incompatibility in mismatched unrelated donor hematopoietic transplants. Killer immunoglobulin-like receptor. Blood 2002;100:3825-3827.
McQueen KL, Dorighi KM, Guethlein LA, Wong R, Sanjanwala B, Parham P. Donor-recipient combinations of group A and B KIR haplotypes and HLA class I ligand affect the outcome of HLA-matched, sibling donor hematopoietic cell transplantation. Hum Immunol 2007;68:309-323.
Méndez A, Granda H, Meenagh A, et al. Study of KIR genes in tuberculosis patients. Tissue Antigens 2006;68:386-389.