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