| 영문 | graft versus host reaction | 한글 | 이식편대 숙주반응 |
|---|---|---|---|
| 설명 | 면역이란 자신의 것과 자신의 것이 아닌 것을 구분해서 자신의 것이 아닌 것을 공격하여 생물학적 활성을 없애거나 제거하는 것이다. 이 면역은 주로 혈액에 있는 세포에 의해서 이루어진다. 특히 림프구는 이 면역에 중추적인 역할을 하는 세포이다. 이식편대숙주반응이라는 것은 이식되어온 조직에 존재하는 타인의 혈구들이 숙주의 세포를 공격하는 것을 말한다. 즉 이식되어온 조직과 함께 들어온 혈구들이 이식을 받은 사람의 세포를 타인의 것으로 인지해서 공격하는 현상이다. 이것은 이식을 받은 사람의 면역상태가 정상적일 경우에는 일어나지 않는데 왜냐하면 면역상태가 정상일 경우에는 이식되어온 장기와 더불어 들어온 타인의 혈구들을 이식을 받은 사람의 혈구가 타인의 것으로 인지해서 공격을 하고 숫적으로 유리하여 모두 죽일 수가 있기 때문이다. |
||
| CRL | cell repository line; Certified Record Librarian; complement receptor location; complement receptor ... |
|---|---|
| CR | calculation rate; calculus removed; calorie-restricted; cardiac rehabilitation; cardiac resuscitatio... |
| CBAB | complement-binding antibody |
| C4BP | complement 4 binding protein |
| Fabc | fragment, antigen and complement binding [of immunoglobulins] |
| complement 3 | The fourth component to attach in the complement reaction sequence. It is a beta-globulin with a sedimentation coefficient of 5.5, a molecular weight of 185,000 and a serum concentration of 1.3 micrograms/ml. Its fragments have anaphylatoxic, chemotactic, and histaminic action and affect smooth muscle. (12 Dec 1998) |
|---|---|
| complement 3a | <chemical> Smaller fragment formed when c3 convertase splits c3 into c3a and c3b. C3a is a 77-amino acid peptide that includes a carboxy-terminal arginine which is crucial for its biological activities. C3a causes symptoms of immediate hypersensitivity (anaphylaxis) including smooth muscle contraction, mast cell histamine release, and local inflammation. It is considered an anaphylatoxin along with c4a, c5a, and c5a des-arginine. Chemical name: Complement C3a (12 Dec 1998) |
| complement 3b | <chemical> The larger fragment formed when c3 convertase splits c3 into c3a and c3b. In both the classical and alternate pathway, c3b participates in immune adherence and enhances phagocytosis. It also forms a cellular intermediate which continues the complement process. In the alternate pathways, c3b initiates a positive feedback activation of c3pase. Chemical name: Complement C3b (12 Dec 1998) |
| complement 3b inactivators | Compounds which inhibit, antagonise, or inactivate complement 3b. A well-known inhibitor is a beta-globulin which cleaves c3b into inactive fragments c3c and c3d. C3bina plays a key role in the regulation of the complement system by blocking the cytolytic sequence and preventing recruitment of the properdin amplification loop. (12 Dec 1998) |
| complement 3c | <chemical> An inactivated form of complement 3b (c3b). Complement 3b is inactivated with the help of two regulatory factors, complement factor h and complement factor I. Complement factor h (c3b inactivator accelerator) makes c3b susceptible to the serine protease, complement factor I (formerly called kaf, c3binf, or enzyme 3b inactivator), to form ic3b. Then complement factor I and a trypsin-like proteolytic enzyme further cleave ic3b into c3c and c3dg. Chemical name: Complement C3c (12 Dec 1998) |
| complement 3 convertase | <enzyme> The enzyme which in both the classical and alternate complement pathways cleaves complement 3 into anaphylatoxin (c3a) and c3b. Registry number: EC 3.4.21.43 (12 Dec 1998) |
| complement 3d | <chemical> An inactivated fragment of complement 3b (c3b). Factor h makes c3b susceptible to factor I (formerly called kaf, c3binf, or enzyme 3b inactivator) to form ic3b. Then factor I and a trypsin-like proteolytic enzyme further cleave ic3b into c3c and c3dg. Serum proteases degrade c3dg into complement 3d (c3d) and c3g. Chemical name: Complement C3d (12 Dec 1998) |
| complement 3 nephritic factor | A magnesium-dependent IgG autoantibody found in serum of patients with chronic mesangioproliferative hypocomplementemic glomerulonephritis. It causes inactivation of c3 in the alternate pathway by cleaving c3 into two inactive fragments, c3c and c3d, instead of the normal c3b. (12 Dec 1998) |
| complement 4 | The second component to react in the complement sequence. It is a beta-globulin with a sedimentation coefficient of 18.7, a molecular weight of 240,000 and a serum concentration of 430 micrograms/ml. It is activated by complement 1 and serves as a receptor for c2. (12 Dec 1998) |
| complement 4a | <chemical> Smaller fragment formed when c1s splits c4 into c4a and c4b. As an anaphylatoxin, c4a causes symptoms of immediate hypersensitivity but it has weaker activity than c3a or c5a. Chemical name: Complement C4a (12 Dec 1998) |
| complement 4b | <chemical> Larger fragment formed when c1s splits c4 into c4a and c4b. C4b combines with c2b to form the activated c4b2b complex which is often called the classical pathway c3 convertase. Chemical name: Complement C4b (12 Dec 1998) |
| complement 5 | The fifth component in the complement reaction sequence, probably exists in a complex with c6 and c7. It is a beta-globulin with a sedimentation coefficient of 10, serum concentration of 75 micrograms/ml and molecular weight of 180,000. It is activated by c423 and releases fragments with anaphylatoxic, chemotactic, and histamine-releasing actions and affecting smooth muscle. (12 Dec 1998) |
| complement 5a | <chemical> Smaller fragment formed when c5 convertase splits c5 into c5a and c5b. C5a is a 74-amino acid peptide that includes a carboxy-terminal arginine crucial for its spasmogenic activity and a carbohydrate moiety. C5a is the most potent anaphylatoxin mediating immediate hypersensitivity. Chemical name: Complement C5a (12 Dec 1998) |
| complement 5a, des-arginine | Complement 5a with the carboxy-terminal arginine removed. The arginine is rapidly cleaved from the c5a fragment during complement activation by carboxypeptidase b present in normal human serum. C5a des-arg shows complete loss of spasmogenic activity though it retains some chemotactic ability. (12 Dec 1998) |
| complement 6 | The sixth component in the complement reaction sequence. It is a beta-globulin with a sedimentation coefficient of 8.7 and a molecular weight of 120,000 at 60 micrograms/ml in serum. It may exist in a complex with c5 and c7 and is activated by the binding of c5. (12 Dec 1998) |