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Una variante de enfermedad autoinmune de IgG1 modula la activación y diferenciación de las células B

Xiangjun Chen¹, Xiaolin Sun², Wei Yang³

¹Ministry of Education Key Laboratory of Protein Sciences, Center for Life Sciences, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Institute for Immunology, School of Life Sciences, Tsinghua University, Beijing 100084, China.

Science (New York, N.Y.)

|October 6, 2018

Resumen

Una variante específica de la inmunoglobulina humana G1 (IgG1), hIgG1- G396R, promueve la autoinmunidad y aumenta la producción de anticuerpos. Este hallazgo es crucial para comprender el lupus y las respuestas de la vacuna.

Área de la Ciencia:

Inmunología
Investigación de la autoinmunidad
Biología molecular

Sus antecedentes:

Mantener las células B autorreactivas en un estado de quietud es vital para prevenir enfermedades autoinmunes.
Se ha identificado una variante específica de la inmunoglobulina humana G1 (IgG1), hIgG1- G396R.
Esta variante muestra una correlación positiva con el lupus eritematoso sistémico.

Objetivo del estudio:

Investigar el papel de la variante hIgG1-G396R en la autoinmunidad y la producción de anticuerpos.
Para aclarar los mecanismos moleculares por los que esta variante influye en las respuestas inmunes.

Principales métodos:

Se utilizaron modelos de lupus inducido con el homólogo murino Gly390Arg (G390R) en ratones knockin.
Se examinó la producción de anticuerpos en ratones inmunizados con hapten G390R y en humanos portadores homocigotos de G396R vacunados contra la gripe.
Se analizó la fosforilación del motivo tirosina de la cola de la inmunoglobulina IgG1 (ITT) y sus vías de señalización aguas abajo.

Principales resultados:

Los ratones G390R generaron un exceso de células plasmáticas y autoanticuerpos de amplio espectro.
Se observó una mayor producción de anticuerpos en ratones portadores de G390R y humanos de G396R después de la vacunación.
La variante potencia la fosforilación del motivo ITT, lo que lleva a un aumento de los tiempos de permanencia de la proteína adaptadora Grb2 y la señalización de la tirosina quinasa (Btk) de hiper-Grb2-Bruton.

Conclusiones:

La variante hIgG1-G396R es un factor significativo en la patogénesis del lupus.
Esta variante juega un papel crucial en la modulación de las respuestas de anticuerpos después de la vacunación.
Comprender el mecanismo de esta variante ofrece información sobre las enfermedades autoinmunes y la eficacia de la vacuna.

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