PATHOPHYSIOLOGY
PREDISPOSING FACTOR PRECIPITATING FACTOR
Age, gender, heredity, race, UNKNOWN Environment, drugs, infection,
hormones, history
ETIOLOGY lifestyle
Female producing estrogen 1st generation familial Influencing agents in the body
possession of influencing SLE
DNA
Increase level of estrogen Similar activity/structure to our
Genetic relational DNA passes own systemic cell
down to ext generation
Unknown cause of estrogen
influencing immune response Human leukocyte antigen class
of the human leukocyte system 1 &2 in chromosome 6
in chromosome 6 possesses multiple genes
influencing in inheriting SLE
Occurrence of SLE activation
Fewer or defective tangible Human leukocyte antigen class
body macrophages in the body 1 &2 in chromosome 6 posses Defect in mechanism of
multiple genes influenced in immune complex clearance
inheriting SLE
Defective clearance of early
apoptotic cell Apoptic chromatin and nuclei
Release of danger signs attach to dendrite
Secondary necrosis of cell
Endocytose of antigen material Defective B cell activation by
by dendritic cell autoantigen
Release of nuclear fragments
as potential auto antigens
Presented to T cells Hyperactivity of defective B cell
Impaired membrane integrity
of dendrite cell
Activation of defective T cell Production of self and non-self
antibodies and B memory cells
Induced maturation of
dendritic cell Production of defective T cells
Negative abnormal B cell
contribution to already
deficient immune system
SYSTEMIC LUPUS
ERYTHEMATOSU
S