Autoimmunity co-signaling system: Regulatory T cells, CTLA-4 and FOXP3

L. M. Gómez Osorio, J. Martín Ibañez, Juan Manuel Anaya Cabrera

Resultado de la investigación: Contribución a RevistaRevisión Literaria

Resumen

Co-signaling molecules can act as co-stimulators or co-inhibitors, depending on whether they promote or suppress T-cell activation, respectively. At the specific time and location, co-signaling molecules positively and negatively control antigen presentation, growth, differentiation and function of T-cells. An important cellular group implicated in the regulation of co-stimulation is known as regulatory T cells (Treg). These cells can be used clinically in treatments ranging from cellular transfer in transplant patients to autoimmune diseases and suppression in cancer patients. Treg act through CTLA-4 molecules, which have the ability to suppress the co-stimulation signals and to stop the T cell response. Recently, CTLA-4Ig fusion molecules have been developed, which can block the presentation of auto-antigens. FOXP3 transcription factor is a specific molecule present in Treg that inhibits the production of IL-2 by CD4+ activated cells. Currently, FOXP3 functions are being extensively studied in order to develop new therapeutic targets. This article reviews co-signaling and its mechanism in Treg (CTLA-4, FOXP3), as well as its role in the physiopathology of autoimmune diseases.
Idioma originalEnglish (US)
Páginas (desde-hasta)283-297
Número de páginas15
PublicaciónInmunologia
EstadoPublished - jul 1 2005

Huella dactilar

Regulatory T-Lymphocytes
Autoimmunity
Antigen Presentation
T-Lymphocytes
Autoimmune Diseases
Interleukin-2
Transcription Factors
Transplants
Therapeutics
Growth
Neoplasms

Citar esto

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title = "Autoimmunity co-signaling system: Regulatory T cells, CTLA-4 and FOXP3",
abstract = "Co-signaling molecules can act as co-stimulators or co-inhibitors, depending on whether they promote or suppress T-cell activation, respectively. At the specific time and location, co-signaling molecules positively and negatively control antigen presentation, growth, differentiation and function of T-cells. An important cellular group implicated in the regulation of co-stimulation is known as regulatory T cells (Treg). These cells can be used clinically in treatments ranging from cellular transfer in transplant patients to autoimmune diseases and suppression in cancer patients. Treg act through CTLA-4 molecules, which have the ability to suppress the co-stimulation signals and to stop the T cell response. Recently, CTLA-4Ig fusion molecules have been developed, which can block the presentation of auto-antigens. FOXP3 transcription factor is a specific molecule present in Treg that inhibits the production of IL-2 by CD4+ activated cells. Currently, FOXP3 functions are being extensively studied in order to develop new therapeutic targets. This article reviews co-signaling and its mechanism in Treg (CTLA-4, FOXP3), as well as its role in the physiopathology of autoimmune diseases.",
author = "{G{\'o}mez Osorio}, {L. M.} and {Mart{\'i}n Iba{\~n}ez}, J. and {Anaya Cabrera}, {Juan Manuel}",
year = "2005",
month = "7",
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language = "English (US)",
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Autoimmunity co-signaling system: Regulatory T cells, CTLA-4 and FOXP3. / Gómez Osorio, L. M.; Martín Ibañez, J.; Anaya Cabrera, Juan Manuel.

En: Inmunologia, 01.07.2005, p. 283-297.

Resultado de la investigación: Contribución a RevistaRevisión Literaria

TY - JOUR

T1 - Autoimmunity co-signaling system: Regulatory T cells, CTLA-4 and FOXP3

AU - Gómez Osorio, L. M.

AU - Martín Ibañez, J.

AU - Anaya Cabrera, Juan Manuel

PY - 2005/7/1

Y1 - 2005/7/1

N2 - Co-signaling molecules can act as co-stimulators or co-inhibitors, depending on whether they promote or suppress T-cell activation, respectively. At the specific time and location, co-signaling molecules positively and negatively control antigen presentation, growth, differentiation and function of T-cells. An important cellular group implicated in the regulation of co-stimulation is known as regulatory T cells (Treg). These cells can be used clinically in treatments ranging from cellular transfer in transplant patients to autoimmune diseases and suppression in cancer patients. Treg act through CTLA-4 molecules, which have the ability to suppress the co-stimulation signals and to stop the T cell response. Recently, CTLA-4Ig fusion molecules have been developed, which can block the presentation of auto-antigens. FOXP3 transcription factor is a specific molecule present in Treg that inhibits the production of IL-2 by CD4+ activated cells. Currently, FOXP3 functions are being extensively studied in order to develop new therapeutic targets. This article reviews co-signaling and its mechanism in Treg (CTLA-4, FOXP3), as well as its role in the physiopathology of autoimmune diseases.

AB - Co-signaling molecules can act as co-stimulators or co-inhibitors, depending on whether they promote or suppress T-cell activation, respectively. At the specific time and location, co-signaling molecules positively and negatively control antigen presentation, growth, differentiation and function of T-cells. An important cellular group implicated in the regulation of co-stimulation is known as regulatory T cells (Treg). These cells can be used clinically in treatments ranging from cellular transfer in transplant patients to autoimmune diseases and suppression in cancer patients. Treg act through CTLA-4 molecules, which have the ability to suppress the co-stimulation signals and to stop the T cell response. Recently, CTLA-4Ig fusion molecules have been developed, which can block the presentation of auto-antigens. FOXP3 transcription factor is a specific molecule present in Treg that inhibits the production of IL-2 by CD4+ activated cells. Currently, FOXP3 functions are being extensively studied in order to develop new therapeutic targets. This article reviews co-signaling and its mechanism in Treg (CTLA-4, FOXP3), as well as its role in the physiopathology of autoimmune diseases.

M3 - Literature review

SP - 283

EP - 297

JO - Inmunologia

JF - Inmunologia

SN - 0213-9626

ER -