Systemic lupus Erythematosus
-
Upload
juan-jose-cano -
Category
Science
-
view
74 -
download
0
Transcript of Systemic lupus Erythematosus
Juan José Cano FernándezValeria Guerra Espinosa
Recent researchs support the important role of the cytokine genes in autoimmune diseases, high serum levels of TNF-alfa and IFN- gamma wich are a very important pro-inflammatory citokines have been reported in SLE, a complex disease that causes a high rate of mortality worldwide.
INTRODUCTION
Is a prototypic autoinmune complex disease which is characterized by excessive production of autoantibodies against a broad range of self-antigens.
For SLE diagnosis, the patient must satisfy at least 4 criteria accordin to the SLE classification
Systemic lupus Erythematosus :
Polymorphism is the occurrence of two or more clearly different morphs or forms, also referred to as alternative phenotypes, in the population of a species.
Is the variation of a gene in a population
Polymorphisms
TNF- α Is a cell signaling
protein (cytokine) involved in systemic inflammation and is one of the cytokines
that make up the acute phase reaction.
the regulation of immune cells endogenous pyrogeninduce fever apoptotic cell death inflammation inhibit viral replication respond to sepsis
Function
IFN-Y Interferon gamma is a
cytokine that is the only member of the
type II class of interferons. The existence of this
interferon, which early in its history was
known as immune interferon
innate and adaptive immunity against viral, bacterial and protozoal infections.
activator of macrophages and
inducer of Class II MHC
Function
Polymorphisms
TNF- α IFN-Y
-308 G>A
+874 A>T
SLE
This article is based on finding how the TNF-alfa and IFN-gamma are associated with immune factors especially in the systemic lupus erythematosus (SLE) and if this genes polymorphism could affect the susceptibility and severity of the diasease.
OBJECTIVE
METODOS Y SUJETOS 125
PACIENTES CON LES (LN)
•72 Mujeres•53 Hombres•23.4 ± 4.4 años
112 PACIENTE
S SALUDAB
LES
•66 Mujeres •46 Hombres•28.3± 6.2 años
Centro de urología y nefrología, universidad
Mansoura ,Egipto.Diagnostico de los
pacientes: criterios de LES de la Universidad
Americana de Reumatología
237 PACIENTES EN TOTAL
CLASIFICACION DE LUPUS NEFRITICO
CLASE I
Glomérulo normal
0 casos
CLASE II
Enfermedad mensagial
pura
8 casos
CLASE III CLASE IV CLASE V
Glomerulonefritis
membranosa
Glomerulonefritis proliferativa
local
Glomerulonefritis
proliferativa difusa
4 casos 88 casos 25 casos
Evaluar la severidad del LN
1. Lisis celular de glóbulos rojos
2. Lisis nuclear
3. Precipitación de ADN
4. Precipitación de proteínas
5. Almacenamiento de ADN
EXTRACIÓN DE ADN
PCR- Reacción en cadena de la Polimerasa
Amplificación directa de un
gen o un fragmento de
DNA
Incremento del numero de copias de una secuencia particular de DNA
1. Desnaturalización2. Hibridación con un
Primer3. Síntesis por la DNA
polimerasa
TNF-α GTNF-α AINF-γ TINF-γ A
PCR- ARMS ARMSSistema de mutación refractaria a la
amplificación
Es un método ideal simple para detectar cambios simples en las bases o pequeñas
delaciones
RESULTADOS
TNF-αEl polimorfismo se detecto a 184Pb.
IFN-YEl polimorfismo se detecto a 263PB
Casos con LES mostraron aumento significativo de TNF- Y IFN- plasmático en comparación con
los controles
Debido a la alta frecuencia de
genotipos heterocigotos
los genotipos homocigóticos no
mostraron diferencia
significativa
Author What they said Yes No
Guarniso-zuccardi et al
Individuals that carrying TNF-α -308ª, risk allele were significantly associated with SLE in European, South American and Mexican subjets but was not associated with SLE in Asian and African subjects
X
Kim et al Analysis of the relationship between the IFN-Y +874 A>T SNP and susceptibility to SLE.
x
The polymorphisms in TNF-α and INF-Y genes increase the susceptibility of individuals to acquire systemic erythematosus lupus
The polymorphisms in TNF-α and INF-Y genes doesn’t generate alteration on the severity disease symptoms.
There are factors like different ethnic origin, diverse genetic and epigenetic interaction that could produce changes in the results.
The TNF-α and INF-Y could be a excellent pharmacology target for the SLE treatment.
CONCLUSSION