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

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

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

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

They produce antibodies in response to an antigen.

Neutrophils and macrophages.

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

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

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

1-2 days.

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

Activated B and plasma cells.

Humoral immunity and cell-mediated immunity.

Severe Acute Respiratory Syndrome Coronavirus 2.

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

HBsAg and viral DNA may reappear.

Years.

To present peptide antigens to CD8+ T cells.

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

Antigen and MHC.

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

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

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

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

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

Tolerance (unresponsiveness) to self-Ag.

Innate immunity.

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

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

The thymus.

Killing of infected cells.

Innate immunity has no memory.

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

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

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

It is the basis of autoimmune diseases.

Degranulation.

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

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

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

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

Two tails.

Natural barriers, phagocytes, and secreted molecules.

To modulate immune responses.

They are where antigens bind.

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

Major functional activity, producing large amounts per cell.

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

They develop regulatory T cells.

Interferon, macrophages, NK cells.

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

Bone marrow.

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

It allows for the binding and presentation of peptide antigens.

Cytotoxic T lymphocytes and Helper T-Cells.

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

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

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

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

Creation of immunologic memory.

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

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

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

To respond to intracellular pathogens.

PRRs recognize PAMPs and DAMPs in innate immunity.

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

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

Live attenuated human or non-human pathogens.

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

It has a large polysaccharide coat.

A mouse is challenged with an antigen.

The hinge region provides flexibility.

Immunoglobulins.

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

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

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

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

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

The presence of an activating ligand due to infected cells.

Cognitive phase, Activation phase, Effector phase.

Pertussis or Influenza.

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

They are formed by fusing spleen cells with myeloma cells.

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

Via disulfide bonds.

Pepsin and Papain.

Injured tissue.

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

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

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

Plasma cells that produce immunoglobulins or antibodies.

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.

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

Recognition of antigen.

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

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

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

Hypoxanthine-aminopterin-thymidine (HAT) medium.

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

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

They are morphologically similar when not activated.

Substances that cause allergic reactions due to failure of tolerization.

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

They present antigens to T cells in lymphoid organs.

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

Secretion of antibodies to eliminate antigens.

Helper T-cells or cytotoxic T-cells.

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

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

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

Yields 2 Fab fragments and 1 Fc fragment.

IgG.

IgG.

Active immunity provides memory, while passive immunity does not.

They can directly kill infected cells.

Activation and proliferation of antigen-specific B cells.

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

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

Multi-protein complexes involved in the acute inflammatory response.

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

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

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

Pentameric.

Because it is too big.

Tetanus toxoid, usually given with an active tetanus vaccine.

Resembles a 'Y' shape.

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

HLA are associated with autoimmune diseases.

It mediates immediate hypersensitivity and defense against worm infections.

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

Elevated in primary responses and most efficient in activating complement.

Maternal IgG transported across the placenta.

The antibody-binding region that recognizes antigens.

It promotes interleukin-associated inflammatory responses.

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

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

To maintain protective antibody levels over time.

IgA.

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

IgM, IgG, IgA, IgE.

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

IFN-𝛾.

Hepatitis B antigen (HBsAg) and viral DNA.

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

The complement-binding site.

Naturally occurring allograft.

3 weeks.

Phagocytosis and bactericidal mechanisms.

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

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

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

Only IgA has a secretory component.

Maternal exposure to fetal antigens during pregnancy.

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

Parasites and they can also appear during allergic reactions.

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

A swollen fetus due to large amounts of fluid buildup.

In the gut mucosa and secretions.

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

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

Macrophage activation and stimulation of IgG antibody production.

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

A group of molecules that share the immunoglobulin domain fold.

Also called fixed macrophages, they maintain homeostasis.

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

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

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

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

They can range from mildly annoying rhinitis to fatal anaphylaxis.

It categorizes cell surface molecules recognized by specific monoclonal antibodies.

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

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

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

Linear (continuous) and conformational (discontinuous).

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

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

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

Cytokines and interleukins that can cause significant inflammation.

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

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

They block virus replication.

Vasoactive amines and lipid mediators.

To trap and kill pathogens extracellularly.