Lecture 11 Immune Responses

Helps ramp up resonse

Used to maintain immunological tolerance. It shuts off the adaptive immune system.

Destroy virus infected cells and tumor cells. It also causes organ transplant rejection. Kills cells with MHC-antigen complexes

Secretes antibodies, presents antigens, secretes cytokines, and expresses B cell receptors.

Help activate B cells via antigen binding

Cytotoxic lymphocyte. They recognize and kill stressed cells when antibodies and MHC is not present. It helps with antibody dependent cytotoxicity, tumor cell surveillance(w/ or w/o MHC), and breaking down senescent cells.

Describes a cell that is winding down and starting to no longer function properly.

Early on, cells with receptors that bind self-antigens are destroyed so only the ones that don’t bind self-antigens end up replicating.

A too clean environment in early childhood contributes to a weakened immune system.

The increase in autoimmune and allergic diseases are because of a lack of microbiome diversity.

1. Vasodilation of local vessels and excess blood flow

2. Increased capillary permeability and fluid leaks to interstitial space

3. Fluid clotting in the interstitial space. Fibrin clotting keeps it there

4. Granulocytes and monocytes migrate into the tissue

5. Swelling

As the immune cell goes by, one of its receptors is bound by a receptor on an epithelial cell as it’s getting ready for diapedesis.

All three receptors are bound so diapedesis can occur.

Histamine, bradykinin, serotonin, reaction products of the complement system, products of blood clotting, and lymphokines.

Macrophages are first to deal with potential infections. Then neutrophils from the blood and there’s a third wave that consists of macrophages. The fourth wave is an increase in granulocyte and monocyte production in the bone marrow.

Acute increase in the number of neutrophils in the blood

Broad, immediate onset, on/off regulation, lower potency, fast, can’t be amplified, quick, and always present.

Specific, 3 day lag in onset, can be amplified, greater potency, slow, and long term response.

Help with rapid response. Some are always present and some are secreted as necessary

Attract phagocytes to site of infection

Proteins that coat pathogens so phagocytes recognize and ingest them. Attracts leukocytes and causes mast cell degranulation.

Fever-producing substances

Vasodilator and bronchoconstrictor released by mast cells and basophils

Secreted in inactive forms and activated as the cascade proceeds. Intermediates of the complement cascade act like opsonins. The membrane attack complex forms at the end.

Forms pore in pathogen membrane so water flows in and it lyses.

Act like opsonins in liver and enhance the inflammatory response

Major histocompatibility complexes. Every nucleated cell has MHC 1 molecules. MHCs combine with peptide fragments of antigens and are inserted into the cell membrane.

Ig G, A, M, E, D. The class is decided by the antibody heavy chain.

Only antigen presenting cells use this..

No organelles, doesn’t need host to survive, singular circular DNA chromosome, and antibiotics work on it.

Nucleic acid core in a protein capsid and some have an external envelope, needs a host, could have DNA or RNA, and antivirals may work.

Epithelium, grandular secretions containing antibodies and enzymes, stomach acidity, and mechanical removal ie cilia.

Redness, heat, swelling, and pain

DAMPs and other chemotaxins

If an infected cell ramps down MHC receptors when the NK cell bumps it, it’ll sense the lack of interaction and kill the cell.

Allows phagocytosis when a bacteria binds to it.

Macrophages and dendritic cells are the main ones

Carries out immediate response

Present for a long time and ramps up lymphocyte expansion when activated

First exposure of a B cell to antigen results in proliferation. Effector cells do their job, plasma cells are made, and LLPCs are made.

Long lived plasma cells that are made in the primary response but used in the secondary. Once exposed to the antigen they create a faster, stronger response.

LLPCs make plasma cells and effector cells for a stronger and longer lasting response.

Antigen clumping to group bacteria together, inactivating toxins by binding them, acting as opsonins to make it easier for bacteria to be phagocytized. Triggering NK or eosinophil degranulation to kill bacteria, activating complements, or activating B cells to make plasma cells and memory cells.

Result of pathogen exposure and making antibodies

Gaining antibodies from another organism. Usually temporary like from mother or donated plasma.

Usually involves pathogen that is recognizable but not harmful.

Antigen presenting cell has an antigen stuck to its MHC 2 receptor and if it encounters a helper T cell it'll create an immune response/cytokines. If the complex was made with MHC 1 that means a cell is infected so if it finds a cytotoxic T cell it’ll be killed.

Bacteria have gotten in so immune cells are fighting the potential infection

Cytotoxic T cells and NK cells

Has its own field called psychoimmunology. There’s overlap in the relationships and they can impact each other.

Graft vs host where graft rejects the host. And host vs graft.