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AUTOIMUNITAS vs
TOLERANSI
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Self-tolerance
Central tolerance: primary lymphoid
organs
High concentration of self-antigens
Clonal deletion = destruksi limfosit
B cell mechanisms
Peripheral tolerance: peripheral
tissue
Lymphocyte
Maturation
Antibody Mediated
Immunity
B Cells Mature
in Marrow
Stem Cells
of the Bone
Marrow
Released into
blood, spleen,
lymph
Identify
Antigens
B Cells Replicate
to form
Plasma cells
B Memory
Cells
Cell Mediated
Immunity
T Cells Mature
in Thymus
Macrophages
carry foreign
cells to T
Helper cells
T Helper cells (Th)
produce proteins
Release
Antibodies
Effector Tc
Cells
Secrete
Interleukins
Secrete
lymphokines
Replicate
Cytotoxic (killer)
T (Tc) Cells
Stimulates
Phagocytosis
Tm Memory
Cells
faal_imun/ikun/2006
Autoimmune Diseases
Failure of autoantibodies and T cells to
recognize own cells
Autoantibodies and T cells launch attack
against own cells
Perhaps due to overactive or an
overabundance of helper T lymphocytes
RESPON IMUN :
NOT SELF
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SELF
- IMUNITAS
- HIPERSENSITIF
- SAKIT
- IMUN TOLERAN
Autoimmunity-mechanisms
Failure of self-tolerance
Molecular mimicry
Release of sequestered antigens
Change in self-antigens
Genetic factors/MHC genes
Hormonal
PATOGENESIS AUTOIMUNITAS
HIPOTESIS:
1.
SEQUESTER ANTIGEN (Ag TERASING)
TOLERANSI JARINGAN JANIN, KECUALI YG TERPISAH SCR
ANATOMIS ( LENSA, TESTIS, SSP ) BILA DEWASA TERPAPAR
INF/TRAUMA RESPON AUTOIMUN
2.
FORBIDDEN CLONE
MUTASI SOMATIK LIMFOSIT YG TIDAK MENGEKSPRESIKAN
ANTIGEN NON-SELF TETAP HIDUP TERJADI RESPON
LIMFOSIT THD JARINGAN TUBUH KERUSAKAN
3.
DEFISIENSI IMUN
HIPOAKTIF ATAU DEFISIENSI SISTIM IMUN
4.
CROSS-REACTION
a. PERUBAHAN STRUKTUR ANTIGEN KARENA:
- OBAT2AN (MIS: -METHYLDOPA THD ERITROSIT)
- INFEKSI VIRUS
b. STUKTUR ANTIGEN NON-SELF = SELF ( MIS: STREPT. DG
MIOKARDIUM DEMAM REMATIK)
Antinuclear antibodies
Against proteins, nucleic acids,
nucleoproteins
3-15% population + at low titers
Detection
Immunofluorescence (Hep2)
ELISA
RIA (gold standard)
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