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Innate Immunity 先天性免疫

Innate Immunity 先天性免疫. Memory ?. The front line of host defense. SP-A & D, defensin (opsonization). colicins of E. coli lactic acid from lactobacilli *antibiotic treatment. Establish an infection. (macrophage). (neutrophil). Macrophages are activated

raymond-osborne
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Innate Immunity 先天性免疫

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  1. Innate Immunity 先天性免疫

  2. Memory ?

  3. The front line of host defense SP-A & D, defensin (opsonization) colicins of E. coli lactic acid from lactobacilli *antibiotic treatment

  4. Establish an infection (macrophage) (neutrophil)

  5. Macrophages are activated by pathogens and both engulf them and initiate inflammatory responses. co-stimulatory molecules (B7)

  6. Neutrophil : short-lived Macrophage : long-lived, continued to generate new lysosomes Genetic deficiency of NADPH oxidase – chronic granulomatous disease

  7. 抑制酸化 阻止融合 Mycobacteria

  8. Macrophages are activated by pathogens and both engulf them and initiate inflammatory responses. co-stimulatory molecules (B7)

  9. Pattern-recognition receptors : A.直接辨識 pathogen，引發吞噬 (phagocytic receptor) Mannose-binding lectin (MBL) : free in plasma 與細菌細胞壁的mannose結合 細菌表面分子的相對位置很重要 opsonization Macrophage mannose receptor : 與細菌及一些病毒 (如HIV) 上的mannose 結合 Scavenger receptors (與老化RBC的清除亦有關) B. 傳遞訊號 (signaling receptor) Toll-like receptor (TLR) : 10種gene

  10. LTA TNF-α interferon TNF-α, IFN-β

  11. adjuvant

  12. Macrophages are activated by pathogens and both engulf them and initiate inflammatory responses. co-stimulatory molecules (B7)

  13. Macrophages release cytokines and chemokines to initiate an inflammatory response 1.血流量增多但變慢 (紅、熱) 3.血管通透性增加(腫、痛) 發炎細胞的到達1.WBC 2.Monocyte 3. Others (eosinophil, lymphpcyte)

  14. Enzyme cascades : (trigger by tissue damage) 1. Kinin system : 產生影響血管的 peptides (如 bradykinin)，使血管通透性增加，plasma proteins 進入”病灶“，阻止病原擴散。  造成疼痛 2. Coagulation system : 形成fibrin clot，阻止病原進入血流。

  15. The complement system : 由不同分子誘發， 但產生相同的作用分子 2. phagocytosis 3. pore 1. chemoattractants 4.清除有問題的細胞

  16. Triggered-enzyme cascade

  17. Classical pathway : initiation by activation of C1 complex

  18. MB-lectin pathway MASP-2: cleavage C4 and C2 MASP-1: uncertain 缺乏MBL者，幼年期易受感染，此時adaptive immunity 尚未成熟，移行抗體已下降。

  19. *C3的活化作用只發生在病原體表面，不會發生於*C3的活化作用只發生在病原體表面，不會發生於 宿主細胞上。 因C4b會與病原表面的蛋白或醣類結合， 若無儘快結合， 則C4b會發生水解，變成不可逆且不具活性，無法形成 C3 convertase。C3b也需儘速結合於病原表面。 C2只在與C4b結合時，才可被C1s切割。

  20. Hydrolysis of C3 causes initiation of the alternative pathway Fluid-phase C3 convertase

  21. Amplification loop

  22. Positive regulatory factor : 缺乏者易感染Neisseria

  23. Ingestion of complement-tagged pathogens by phagocytes is mediated by receptors (CR) for bound complement proteins.

  24. 6 types of complement receptors

  25. Anaphylactic shock (anaphylatoxin)

  26. The terminal complement proteins polymerize to form pores in membranes that can kill the pathogens membrane-attack complex C8 = C8 (bind) +C8- (insert)

  27. Neisseria

  28. Complement control proteins regulate all three pathways and protect the host from its destructive effects (serpin) Hereditary angioneurotic edema excess cleaved C4 and C2 fragmentsC2b C2 kinin

  29. Induced innate responses to infection local and distant effects

  30. cysteine CXCR1-6

  31. CCR1-9

  32. Chemokines 的功能及特性 1. 一種chemokine可與一種以上的receptor結合，即可被 多種receptor 辨識。 2. 一種chemokine可由多種不同細胞產生且可影響多種細胞 3. 引起趨化反應，藉由濃度梯度引導effector cells 聚集於 感染部位。 4. 有些種類與淋巴球的發育、移行及血管生成有關。

  33. Adhesion molecules : 3 family C5a TNF- LPS subunit TNF-

  34. Neutrophils leave the blood and migrate to sites of infection in a multistep process mediated through adhesive interactions. fast

  35. extravasation slow 往濃度高處移動 (peaks within first 6 hrs)

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