PATHOPHYSIOLOGY

PREDISPOSING FACTOR PRECIPITATING FACTOR

Age, gender, heredity, UNKNOW Environment, drugs,
race, hormones, history
N infection, lifestyle

ETIOLOG

Female producing 1st generation familial Influencing agents in the

estrogen possession of influencing body
SLE DNA

Increase level of Similar activity/structure

estrogen Genetic relational DNA to our own systemic cell
passes down to ext
generation

Unknown cause of
estrogen influencing
immune response of the
human leukocyte system
in chromosome 6
Human leukocyte
antigen class 1 &2 in
chromosome 6
possesses multiple
genes influencing in

Occurrence of SLE
activation

Fewer or defective Human leukocyte

tangible body antigen class 1 &2 in
macrophages in the chromosome 6 posses
multiple genes
influenced in inheriting
Defective clearance of
early apoptotic cell
Release of danger signs
Defect in mechanism of
immune complex
clearance
Apoptic chromatin and
nuclei attach to dendrite

Secondary necrosis of
cell
Endocytose of antigen Defective B cell
material by dendritic cell activation by
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 Production of self and
cell 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
ERYTHEMAT
OSUS