نماذج مناعه الدكتوره اروى

Types of APCs

Professional APCs:
🛑express both MHC class 1 & 2

🛑They include B cell,DCs,Macrophage

🛑They active CD4&CD8

📛📛📛📛📛

Non professional APCs:

🛑express only the MHC class1

🛑They include all nucletide cells

🛑They activate only CD8


مقارنه ذكرته الدكتوره ومش موجود ضمن مقارنات اللجنه العلميه

●Lymph nodes help in response to antigens in the TISSUES.

● Spleen helps in response for antigens carried by BLOOD.

● Mucosal-associated lymphoid tissues (MALTs) They help in response to antigens at MUCOSAL SURFACES.

Effector B cell or activated B cells or plasma cells
are the only cells that are capable of producing antibodies.

NATURAL Killer cells (NK cells) They are the only type of lymphocytes that provide NATURAL immunity They are *CD56 POSITIVE .

Site of infection

Microbes may be found in

1. Extracellular: attached to the human cells on epithelial surface like cholera or not attached to human cells( in interstitial spaces, blood and lymph ) like staphylococcus aureus.

2. Intracellular: present free in the cytoplasm like viruses or enclosed inside vesicles like mycobacterium of TB.

Functions of the complement proteins:

1- Lysis of the microbes by MAC

2- Promotion of phagocytosis of microbes (oposonization) by C3b.


3- Induction of inflammation by C3a & C5a.

4- Attraction of the inflammatory cells to the site of infection by C3a & C5a.

5- Clearance of immune complexes by phagocytes by CR1 & C3b.

How RBCs help in immunity?

CR1 expressed on erythrocytes aids in the transport of immune complexes to the liver and spleen for degradation by phagocytes.

حسب رأيي الدكتورة ما جاوبت عليه

C1 inhibitor (C1INH) is a protease inhibitor that displaces active C1r2s2 from C1q and
inhibits MASP-1 and MASP-2 of the lectin pathway.

Also called C1q binding protein

It is similar to C4.

👉It produced by the MICROBES.

👉Its deficiency lead to HEREDITARY ANGIOEDEMA ➡ increase activation of classical and lectin pathways ➡ over immune response.

👉Gram positive bacteria can't be killed by MAC so we use C3b to kill it by phagocytosis.

👉Because CR1 which present on the surface of phagocytes has high affinity for C3b and C4b which coat antigens .

👉C3b deficiency ➡ immune complex diseases due to deposition of immune complexes which not cleared by C3b.
👉Also lead to increase infection of capsulted bacteria.

👉Adhesion mediated by CR3 & CR4.
👉Oposonization mediated by CR1 & CR3.

1-Tickover activation
active in HEALTHY people.
2- Membrane bound cascade active only in INFECTED people.