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adalah kumpulan 9 protein plasma bukan antibodi yang diperlukan pada reaksi antigen -

antibodi sehingga terjadi kerusakan jaringan atau kematian mikroba serta lisis sel. Fungsi
terpenting : mediator berbagai proses peradangan a.l : vasodilatasi, pengeluaran cairan,
kemotaksis fagosit dll. Jadi aktivasi komplemen diperlukan untuk dapat terjadinya kerusakan
jaringan serta komponen penting pada reaksi imun tipe II dan tipe III
Ada tiga kategori fungsi sitokin dalam system imun yaitu:

o Sitokin sebagai mediator dan regulator respon imun alami

o Sitokin sebagai mediator dan regulator respon imun didapat

o Sitokin sebagai stimulator hematopoiesis

1) meregulasi respon imun spesifik 2) memfasilitasi respon imun natural 3) mengaktifkan respon

inflamatori 4) mempengaruhi migrasi leukosit 5) menstimulasi hematopoisis.


any of various soluble protein mediators released by sensitized lymphocytes on contact with antigen, and
believed to play arole in macrophage activation, lymphocyte transformation, and cell-mediated IMMUNITY. I
t regulates IMMUNE
RESPONSESthrough differentiation, amplification, and inhibition of cell functions. Lymphokines may also ha
ve a cytotoxic effectorfunction. Used as biologic response modifiers in the treatment of cancer.

IgM is very effective at killing bacteria.


IgA concentrates in body fluidstears, saliva, the secretions of the respiratory tract
and the digestive tractguarding the entrances to the body.
IgE, whose natural job probably is to protect against parasitic infections, is the
villain responsible for the symptoms of allergy.
IgD remains attached to B cells and plays a key role in initiating early B-cell
response.
1. IgM is the immediate antibody that is produced once a human body
is exposed to a bacteria, virus or a toxin
2. IgG is found throughout the body, mainly in most of the bodily
fluids, while IgM is found mainly in the blood and lymphatic fluids.
3. IgM is larger in size compared to IgG
4. IgM is temporary and disappears after a few weeks. It is then
replaced by IgG

IgG

1. Increases in:

a) Chronic granulomatous infections


b) Infections of all types
c) Hyperimmunization
d) Liver disease
e) Malnutrition (severe)
f) Dysproteinemia
g) Disease associated with hypersensitivity granulomas, dermatologic disorders, and
IgG myeloma
h) Rheumatoid arthritis
2. Decreases in:

a) Agammaglobulinemia
b) Lymphoid aplasia
c) Selective IgG, IgA deficiency
d) IgA myeloma
e) Bence Jones proteinemia
f) Chronic lymphoblastic leukemia

IgM

1. Increases (in adults) in:

a) Waldenstrm's macroglobulinemia
b) Trypanosomiasis
c) Actinomycosis
d) Carrin's disease (bartonellosis)
e) Malaria
f) Infectious mononucleosis
g) Lupus erythematosus
h) Rheumatoid arthritis
I) Dysgammaglobulinemia (certain cases)
Note: In the newborn, a level of IgM above 20 ng./dl is an indication of in utero
stimulation of the immune system and stimulation by the rubella virus, the
cytomegalovirus, syphilis, or toxoplasmosis.

2. Decreases in:

a) Agammaglobulinemia
b) Lymphoproliferative disorders (certain cases)
c) Lymphoid aplasia
d) IgG and IgA myeloma
e) Dysgammaglobulinemia
f) Chronic lymphoblastic leukemia

IgA

1. Increases in:
a) Wiskott-Aldrich syndrome
b) Cirrhosis of the liver (most cases)
c) Certain stages of collagen and other autoimmune disorders such as rheumatoid
arthritis and lupus erythematosus
d) Chronic infections not based on immunologic deficiencies
e) IgA myeloma

2. Decreases in:

a) Hereditary ataxia telangiectasia


b) Immunologic deficiency states (e.g., dysgammaglobulinemia, congenital and
acquired agammaglobulinemia, and hypogammaglobulinemia)
c) Malabsorption syndromes
d) Lymphoid aplasia
e) IgG myeloma
f) Acute lymphoblastic leukemia
g) Chronic lymphoblastic leukemia

IgD

1. Increases in:

a) Chronic infections
b) IgD myelomas

IgE

1. Increases in:

a) Atopic skin diseases such as eczema


b) Hay fever
c) Asthma
d) Anaphylactic shock
e) IgE-myeloma

2. Decreases in:

a) Congenital agammaglobulinemia
b) Hypogammaglobulinemia due to faulty metabolism or synthesis of
immunoglobulins
Agammaglobulinemia is a rare disorder that mainly affects males. It is caused by a gene defect that blocks the growth
of normal, mature immune cells called B lymphocytes.

As a result, the body makes very little (if any) immunoglobulins in the bloodstream. Immunoglobulins play a major
role in the immune response, which protects against illness and infection.

Persons with agammaglobulinemia repeatedly develop infections, especially bacterial infections such as Hemophilus
influenzae , pneumococci ( Streptococcus pneumoniae ), and staphylococci. Common sites of infection include:
Gastrointestinal tract
Joints
Lungs
Skin
Upper respiratory tract

Agammaglobulinemia is inherited, which means other people in your family may have the condition.

Symptoms include frequent episodes of:


Bronchitis
Chronic diarrhea
Conjunctivitis (eye infection)
Otitis media (middle ear infection)
Pneumonia
Sinusitis
Skin infections
Upper respiratory tract infections

Infections typically appear in the first 4 years of life.

Other symptoms include:


Bronchiectasis (a disease in which the small air sacs in the lungs become damaged and enlarged)
Unexplained asthma

The immune system uses antibodies to


recognize and fight infections. A
mothers antibodies protect her child
during the first six months of the childs
life. After six months, a child must
produce their own antibodies. Children
with AGMX cant produce their own
antibodies. This leaves them open to
disease.
Symptoms of AGMX usually appear
when children are between six and nine
months old. Some children dont have
symptoms until theyre between three
and five years old. Boys generally show
symptoms at an earlier age.
Aktivasi Komplemen
Sistem komplemen dapat diaktifkan melalui 3 jalur, yaitu jalur lektin, jalur klasik, dan jalur
alternatif.

1. Jalur klasik
Aktivasi komplemen melalui jalur klasik dimulai dengan dibentuknya kompleks antigen-antibodi
larut atau dengan ikatan antibodi dan antigen pada sasaran cocok, seperti sel bakteri. Aktivasi jalur
klasik dimulai dengan C1 yang dicetuskan oleh kompleks imun antibody dan antigen.

2. Jalur Alternatif
Aktivasi jalur alternatif memproduksi produk aktif seperti halnya dengan jalur klasik, tetapi
untuk awal reaksi tidak diperlukan kompleks antigen-antibodi. Aktivasi jalur alternatif dimulai
dengan C3 yang merupakan moleku tidak stabil dan terus menerus ada dalam aktivasi spontan
derajat rendah dan klinis yang tidak berarti. Aktivasi spontan C3 diduga terjadi pada permukaan sel,
meskipun sel normal mengekspresikan inhibitor permukaan yang mencegah aktivasi C3.

3. Jalur Lektin
Lektin adalah protein larut yang mengenal dan mengikat residu manosa dari hidrat arang yang
merupakan bagian dinding sel mikroba. Oleh karena itu jalur lektin disebut jalur MBL (Mannan
Binding Lectin) atau jalur ikatan mannan. Lektin adalah golongan famili kolektin, yang merupakan
protein fase akut dan kadarnya meningkat pada respons inflamasi. Aktivasi jalur lektin diawalai oleh
terjadinya ikatan antara polisakarida mikroba dengan lektin dalam sirkulasi.

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