Lecture 11 Immune Responses

Helper T Cells

Helper T Cells

Helps ramp up resonse

Regulatory T Cells

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

Cytotoxic T Cell

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

B Lymphocytes or B Cells

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

B Cell Receptors

Help activate B cells via antigen binding

Natural Killer Cells

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.

Senescent

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

Recognition of Self

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

Hygiene Hypothesis

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

Microbiome Hypothesis

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

Inflammation Steps

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

Rolling Adhesion

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.

Tight Binding

All three receptors are bound so diapedesis can occur.

What chemicals causes inflammation?

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

Immune Cells in Inflammation

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.

Neutrophilia

Acute increase in the number of neutrophils in the blood

Innate Immune Response

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

Adaptive Immune Response

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

Innate Immune System Molecules

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

Chemotaxins

Attract phagocytes to site of infection

Opsonins

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

Pyrogens

Fever-producing substances

Histamine

Vasodilator and bronchoconstrictor released by mast cells and basophils

Complement Proteins

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.

Membrane Attack Complex

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

Acute Phase Proteins

Act like opsonins in liver and enhance the inflammatory response

MHC stands for

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

Antibody/Immunoglobulin Classes

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

MHC 2

Only antigen presenting cells use this..

Bacteria

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

Viruses

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.

Barriers

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

Hallmarks of Inflammation

Redness, heat, swelling, and pain

Encourages Leukocyte invasion via positive feedback

DAMPs and other chemotaxins

MHC 1 Receptors and NK Cells

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.

Pattern Recognition Receptors

Allows phagocytosis when a bacteria binds to it.

Antigen Presenting Cells

Macrophages and dendritic cells are the main ones

Effector Cells

Carries out immediate response

Memory Cells

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

Primary Immune Response

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

LLPCs

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.

Secondary Immune Response

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

Antibody Uses

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.

Active Immunity

Result of pathogen exposure and making antibodies

Passive Immunity

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

Artificial Active Immunity

Usually involves pathogen that is recognizable but not harmful.

MHC-Antigen Complex

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.

Lymph nodes swell when

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

Good against viruses

Cytotoxic T cells and NK cells

Neuro-Endocrine-Immune Interactions

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

Types of Rejection

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