[BCH LEC - LE 1] 10 - Immunology (V2)

Phagocytes, dendritic cells, complement, and natural killer (NK) cells.

Humoral immunity and cell-mediated immunity.

Many different strains may arise within a patient even over a period of just a few months.

They may downregulate MHC or prevent apoptosis, compromising the innate response and immunologic memory.

They have waxy coats and secrete catalase to block the respiratory burst.

Larger antigens bind in a groove, such as linear peptide epitopes.

Cognitive phase, Activation phase, Effector phase.

1. Dendritic cell with antigen 2. Recognition in lymphoid organs 3. Differentiated effector and memory T cells enter circulation 4. Migration to the site of antigen leading to cytokine secretion or macrophage activation.

To counter or help duplicate and elicit an immune response to the spike protein.

They activate macrophages and lead to inflammation, as well as the proliferation and differentiation of T and B lymphocytes.

Killing of infected cells.

NK cells do not need previous exposure to an antigen to kill infected cells, while CTLs require prior recognition.

Pathogen-Associated Molecular Patterns, which are conserved molecular structures specific to foreign microorganisms.

To respond to intracellular pathogens.

Immunity that can be brought about by exposure to infection or having the infection yourself.

Injured tissue.

There is still a level of antibody effective until 60 years after vaccination.

Helper T-cells or cytotoxic T-cells.

Multi-protein complexes involved in the acute inflammatory response.

Elevated in primary responses and most efficient in activating complement.

Hepatitis B antigen (HBsAg) and viral DNA.

Parasites and they can also appear during allergic reactions.

Cell surface molecules exposed on leukocytes relevant for the immune system.

By B cells and T cells, with adjacent amino acid residues.

They produce antibodies in response to an antigen.

HBsAg and viral DNA may reappear.

Type 1: Intracellular pathogens, Type 2: Surface arthropods, Type 3: Extracellular pathogens.

A substance that causes an immune response by itself, e.g., HBsAg.

Interferon, macrophages, NK cells.

A substance recognized by the adaptive immune system but programmed not to elicit a response, e.g., peanuts.

They coat themselves in host antigens and secrete protease inhibitors to block gut enzymes.

A response initiated against one antigen can prime others, leading to the activation of additional antigens and exacerbation of autoimmune diseases.

NLRs are cytoplasmic sensors that recognize bacterial, viral, parasitic, and fungal PAMPs and form inflammasomes.

Activation and proliferation of antigen-specific B cells.

HLA are associated with autoimmune diseases.

IgM, IgG, IgA, IgE.

Only IgA has a secretory component.

Linear (continuous) and conformational (discontinuous).

Neutrophils and macrophages.

Years.

It is a soluble protein required for folding and expression of the Class I molecule.

Mycobacteria (e.g., tuberculosis), viruses, protozoa.

They suppress the immune response, especially when the threat is eliminated.

Allergies or failure to respond to activation, causing problems with antigen recognition.

Immunoglobulins.

Via disulfide bonds.

It is the main antibody in the secondary response, opsonizes bacteria, fixes complement, neutralizes toxins and viruses, and crosses the placenta.

Secretion of antibodies to eliminate antigens.

MHCs are involved in the presentation of antigens to T-cells.

It mediates immediate hypersensitivity and defense against worm infections.

Granulocytes, including neutrophils and eosinophils, involved in the immune response.

Maternal exposure to fetal antigens during pregnancy.

Also called fixed macrophages, they maintain homeostasis.

It binds to organisms to induce cell death via lysis and produces opsonins to facilitate phagocytosis.

The presentation of an antigen by dendritic cells to T-lymphocytes.

To present peptide antigens to CD8+ T cells.

The thymus.

Specialized for degradation and proliferation of particulate antigens to T-cells.

Bone marrow.

Vaccines, natural immunity to microbes, successful transplantation, and monoclonal antibodies.

Nonself antigens from members of the same species, e.g., in graft rejection.

Pepsin and Papain.

Hypoxanthine-aminopterin-thymidine (HAT) medium.

Functions as a receptor, internalizes, degrades, and presents antigens to T cells.

There is an increased response; faster and higher levels of antibody are produced.

IFN-𝛾.

IgE, which is bound to Fc on mast cells and basophils.

It can lead to antibody secretion, class switching, affinity maturation, and production of memory B cells.

It develops 2-24 hours after exposure and is triggered by cytokines and chemokines, leading to leukocyte infiltration and bronchospasm.

It indicates the presence of antibodies after infection and helps monitor viral load.

Using existing vaccines against polio virus or tuberculosis to elicit a general immune response.

A condition where the immune system fails to have the right mix of immune elements.

To modulate immune responses.

Cytotoxic T lymphocytes and Helper T-Cells.

They can circulate and find their way into secondary lymphoid organs.

Naive cell, activated lymphocyte, effector lymphocyte, memory lymphocyte.

By receiving a vaccine, which can provide specificity and memory during recovery.

Forms a fragment of F(ab’)2 and a degraded Fc fragment.

It prevents the attachment of bacteria and viruses to mucous membranes.

A slow primary response with a low level of antibody produced.

The antibody-binding region that recognizes antigens.

The complement-binding site.

A swollen fetus due to large amounts of fluid buildup.

The release of arachidonic acid, forming Prostaglandin A2 and Leukotrienes.

Activated B and plasma cells.

To present antigens to T-cells, initiating the adaptive immune response.

Because the virus can mutate, making the previous vaccine ineffective against new strains.

They are where antigens bind.

Haptens bind in a crevice or pocket, such as Vitamin K.

Live attenuated human or non-human pathogens.

The presence of an activating ligand due to infected cells.

Plasma cells that produce immunoglobulins or antibodies.

Substances that cause allergic reactions due to failure of tolerization.

Yields 2 Fab fragments and 1 Fc fragment.

Pentameric.

Class I MHC molecules are expressed on all nucleated cells and platelets and are recognized by CD8+ lymphocytes.

3 weeks.

It indicates a secondary immune response and is present several months after infection.

They can range from mildly annoying rhinitis to fatal anaphylaxis.

They block virus replication.

1-2 days.

Innate immunity is non-specific and has a fast response, while adaptive immunity is specific and has a slow response.

It allows the immune system to respond more rapidly and effectively upon re-exposure to the same pathogen.

Natural barriers, phagocytes, and secreted molecules.

It allows for the binding and presentation of peptide antigens.

PRRs recognize PAMPs and DAMPs in innate immunity.

Damage-Associated Molecular Patterns, which are endogenous danger molecules released from damaged or dying cells.

Self antigens from normal host molecules, e.g., in systemic lupus erythematosus (SLE).

Infectious microbes may contain antigens that mimic self antigens, causing the immune response to react against self.

MHC molecules display peptide fragments of protein antigens for recognition by antigen-specific T-cells.

Maternal IgG transported across the placenta.

Class II MHC molecules are expressed on cells that present ingested antigens and respond to T-cell help, recognized by CD4+ lymphocytes.

Recruitment of neutrophils and monocytes, and host defense against extracellular bacteria and fungi.

A 110 amino acid polypeptide folded to create antiparallel beta pleated sheets held by intrachain disulfide bonds.

Cytokines and interleukins that can cause significant inflammation.

The formation of different cellular elements of the blood from stem cells to mature forms.

Severe Acute Respiratory Syndrome Coronavirus 2.

NS-1 is used to detect dengue viremia during the first 3 to 5 days of infection.

Major functional activity, producing large amounts per cell.

It is the biologic effector region that binds to various cellular receptors and complement.

It has a large polysaccharide coat.

Pertussis or Influenza.

Every B or T-cell expresses a different antigen recognition molecule created from multiple gene segments that undergo somatic rearrangement.

IgG.

Tetanus toxoid, usually given with an active tetanus vaccine.

To maintain protective antibody levels over time.

IgM is present early after infection as part of the primary immune response.

Macrophage activation and stimulation of IgG antibody production.

Antigen receptors on T & B lymphocytes, antigen-presenting molecules, NK cell receptors, and co-receptors on T-cells.

To trap and kill pathogens extracellularly.

It refers to how pathogens develop evasion mechanisms despite the adaptive immune response, leading to the development of different vaccines.

Antigen and MHC.

Innate immunity has no memory.

Two tails.

They have a wide variety of uses in diagnostics and therapeutics.

The NK cell is not activated, resulting in no cell killing.

MHC is polygenic and polymorphic, existing in different types of cells and exhibiting diversity.

TLRs are transmembrane proteins that recognize a broad range of specificities including proteins, nucleic acids, and glycans.

They are morphologically similar when not activated.

It indicates that the antibody is fully derived from mouse cells.

It is produced in the primary response to an antigen, fixes complement, and serves as an antigen receptor on B-cells.

It promotes interleukin-associated inflammatory responses.

Naturally occurring allograft.

In the gut mucosa and secretions.

They induce apoptosis of virally infected or tumor-damaged cells without needing priming.

By B cells, created from amino acid residues in different parts of the polypeptide chain.

Innate immunity has a brief onset (within hours), while adaptive immunity has a slower onset (1-5 days).

They use RNA polymerase, an error-prone enzyme, leading to frequent mutations in the antigenic peptide sequence.

Tolerance (unresponsiveness) to self-Ag.

It is the basis of autoimmune diseases.

A substance that can bind to immunologic receptors but cannot elicit an immune response by itself.

A mouse is challenged with an antigen.

An epitope that binds to an extended surface site, typically found on folded proteins like lysosomes.

Recognition of antigen.

Immunity achieved by injecting antibodies from an immune individual into an uninfected individual.

Active immunity provides memory, while passive immunity does not.

Resembles a 'Y' shape.

IgA.

IL-4, IL-5, IL-13.

A condition that exhibits cystic hygroma and can lead to hydrops fetalis.

They capture protein antigens and present peptides for T lymphocyte recognition.

Innate immunity.

Degranulation.

They develop regulatory T cells.

Creation of immunologic memory.

The hinge region provides flexibility.

They are formed by fusing spleen cells with myeloma cells.

A process that enhances the ability of phagocytes to engulf and destroy pathogens.

They present antigens to T cells in lymphoid organs.

They can directly kill infected cells.

The presence of pathogenic bacteria, damaged mitochondria, or fragments like extracellular ATP.

Can cross the placenta, binds to viruses, and neutralizes viruses and toxins.

The T-cell receptor structure is comparable to a membrane-bound Fab fragment, consisting of alpha and beta chains.

A group of molecules that share the immunoglobulin domain fold.

Dendritic cells present the antigen to naive T-cells or B cells, leading to T H 2 cell production.

IgG.

Because it is too big.

Two light chains and two heavy chains, with each chain having variable and constant regions.

Phagocytosis and bactericidal mechanisms.

Involved in phagocytosis, bactericidal mechanisms, and antigen presentation to T-cells.

It categorizes cell surface molecules recognized by specific monoclonal antibodies.

Vasoactive amines and lipid mediators.