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Mecanismos de producción de la enfermedad 97<br />

© ELSEVIER. Fotocopiar sin autorización es un delito.<br />

destruida con formalina. Se prepararon células B específicas de antígeno a<br />

partir de esplenocitos mediante la unión de células CD43+ a placas de Petri<br />

recubiertas con anticuerpo anti-CD43 para eliminar las células T, y las células<br />

no unidas se pasaron a través de una columna de lana de nailon para<br />

deplecionar las células accesorias. Las células retenidas se recogieron y se<br />

unieron a placas de Petri recubiertas con A. actinomycetemcomitans para<br />

enriquecer las células B unidas a A. actinomycetemcomitans (AAB, A. actinomycetemcomitans-binding<br />

B cells). También se recogieron las células B<br />

no unidas a A. actinomycetemcomitans (ANB, A. actinomycetemcomitansnon<br />

binding B cells) y las células B de los ratones donantes no inmunizados<br />

(NIB, non-immunized B cells). Cada tipo de célula B se inyectó en un grupo<br />

de ratones receptores, que fueron infectadas por vía oral con A. actinomycetemcomitans<br />

viable.<br />

Al final, los valores de anticuerpos contra A. actinomycetemcomitans en<br />

suero y líquido crevicular fueron significativamente mayores en los ratones<br />

receptores a los que se les transfirió AAB en comparación con los<br />

ratones receptores a los que se les transfirió ANB o NIB. Se observó un<br />

número notablemente elevado de células formadoras de anticuerpos en el<br />

bazo de los ratones receptores con AAB, y estos ratones también mostraron<br />

una resorción ósea significativamente elevada en comparación con los otros<br />

grupos. Estos resultados sugieren que las células B pueden contribuir a la<br />

resorción ósea periodontal y que para que ésto se produzca se necesita<br />

la estimulación antigénica de las células B.<br />

Kawai et al. (2007) examinaron si la inducción de una respuesta inmunitaria<br />

adaptativa contra la colonización oral de Pasteurella pneumotropica no<br />

patogénica, mediante la inmunización con la bacteria estrechamente relacionada<br />

desde el punto de vista filogenético A. actinomycetemcomitans, podría<br />

provocar una pérdida de hueso periodontal en ratones. La inducción de esta<br />

respuesta adaptativa provocaba una pérdida de hueso periodontal dependiente<br />

del RANKL en los ratones.<br />

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