B- and T-cell memory

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B- and T-cell memory

Foundations

Foundations

Introduction to the immune system
Innate immune system
Complement system
Contracting the immune response and peripheral tolerance
Cytokines
Monoclonal antibodies
Antibody classes
Bacterial structure and functions
B-cell development
B-cell activation, differentiation, and contraction
T-cell development
T-cell activation
B- and T-cell memory
MHC class I and MHC class II molecules
Thymus histology
Cell cycle
Mitosis and meiosis
DNA replication
DNA damage and repair
DNA mutations
Cell membrane
Free radicals and cellular injury
Hypoxia
Necrosis and apoptosis
Inflammation
Crohn disease
Gout
Gout and pseudogout: Pathology review
Inclusion body myopathy
Inflammatory bowel disease: Pathology review
Papulosquamous and inflammatory skin disorders: Pathology review
Myasthenia gravis
Systemic lupus erythematosus
Type I hypersensitivity
Type II hypersensitivity
Type III hypersensitivity
Type IV hypersensitivity
Serum sickness
Anaphylaxis
Graft-versus-host disease
Systemic lupus erythematosus (SLE): Pathology review
Pemphigus vulgaris
Stevens-Johnson syndrome
Rheumatic heart disease
Heart failure: Pathology review
Thrombosis syndromes (hypercoagulability): Pathology review
Body fluid compartments
Movement of water between body compartments
Hyponatremia
Pulmonary edema
Lymphedema
Coagulation (secondary hemostasis)
Platelet plug formation (primary hemostasis)
Erythropoietin
Hemophilia
Coagulation disorders: Pathology review
Platelet disorders: Pathology review
Blood components
Protein C deficiency
Protein S deficiency
Metaplasia and dysplasia
Multiple endocrine neoplasia: Pathology review
Oncogenes and tumor suppressor genes
Amyloidosis
Atrophy, aplasia, and hypoplasia
Environmental and chemical toxicities: Pathology review
Medication overdoses and toxicities: Pathology review
Multiple endocrine neoplasia
Substance misuse and addiction: Clinical
Toxidromes: Clinical
Deep vein thrombosis and pulmonary embolism: Pathology review
Heparin-induced thrombocytopenia
Myocardial infarction
Shock
Arterial disease
Atherosclerosis and arteriosclerosis: Pathology review
Carbohydrates and sugars
Childhood nutrition and obesity: Information for patients and families (The Primary School)
Fat-soluble vitamin deficiency and toxicity: Pathology review
Folate (Vitamin B9) deficiency
Iron deficiency anemia
Osteomalacia and rickets
Vitamin B12 deficiency
Water-soluble vitamin deficiency and toxicity: B1-B7: Pathology review
Wernicke-Korsakoff syndrome
Zinc deficiency and protein-energy malnutrition: Pathology review
Burns: Clinical
Burns
Hyperplasia and hypertrophy
Down syndrome (Trisomy 21)
Edwards syndrome (Trisomy 18)
Patau syndrome (Trisomy 13)
Klinefelter syndrome
Turner syndrome
Angelman syndrome
Prader-Willi syndrome
Fragile X syndrome
DiGeorge syndrome
Phenylketonuria (NORD)
Homocystinuria
Maple syrup urine disease
Disorders of fatty acid metabolism: Pathology review
Ornithine transcarbamylase deficiency
Post-transplant lymphoproliferative disorders (NORD)
Cytomegalovirus infection after transplant (NORD)
Epigenetics
Gene regulation
Independent assortment of genes and linkage
Inheritance patterns
Mendelian genetics and punnett squares
Evolution and natural selection
Antiphospholipid syndrome
Celiac disease
Graves disease
Multiple sclerosis
Diabetes mellitus
Chronic granulomatous disease
Immunodeficiencies: Clinical
Immunodeficiencies: Phagocyte and complement dysfunction: Pathology review
Immunodeficiencies: Combined T-cell and B-cell disorders: Pathology review
Immunodeficiencies: T-cell and B-cell disorders: Pathology review
Candida
Mycobacterium tuberculosis (Tuberculosis)
Tuberculosis: Pathology review
Pneumonia: Pathology review
Pneumonia
Salmonella (non-typhoidal)
Viral structure and functions
Hepatitis medications
Herpesvirus medications
Neuraminidase inhibitors
HIV (AIDS)
Nucleoside reverse transcriptase inhibitors (NRTIs)
Integrase and entry inhibitors
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Protease inhibitors
Vaccinations: Clinical
The flu vaccine: Information for patients and families
Vaccinations

Transcript

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B- and T-cell memory Your immune system is like the military - with two main branches, the innate immune response and the adaptive immune response. Key features of the innate immune response are that the cells are non-specific, meaning that they don’t distinguish one invader from another invader; the response is really fast - occurring within minutes to hours; and there’s no memory associated with innate responses. The adaptive response, which is mediated by lymphocytes like B and T cells - is the opposite of the innate immune response. B and T cells have unique receptors - the B cell receptor and T cell receptor - that differentiate pathogens from each other using their unique parts - called antigens.

These receptors are developed while the T cell or B cell is developing in the bone marrow for B cells or thymus for T cells. Once the cell has a unique antigen-specific receptor expressed on its surface it begins traveling through the lymphatic system - passing through lymph nodes in search for the one antigen that fits the receptor perfectly. If they encounter that antigen, a signal gets delivered to the cell’s nucleus that leads to clonal expansion. That’s where a single T cell or B cell replicates over and over - creating an army of clones that can combat the pathogen. Once the immune response is complete, many of these cells die by apoptosis restoring the immune response to its original size - with one major change. Some of the B and T cells become memory cells, which are basically a pool of lymphocytes that are all set to combat the pathogen, if they encounter it again!

Immunologic memory is sometimes referred to as a secondary or anamnestic response, and it’s different from the primary response. During the primary response a small number of naive B and T cells require activation before they can respond to the pathogen. And activating those B and T cells requires a relatively high pathogen burden and can take days to weeks. And the innate response is really important to fill the gap while the adaptive response is being mounted.

In the secondary response, the memory B and T cells, as well as antibodies, are already made, and it takes a relatively low pathogen burden to re-engage the adaptive immune response. As a result, the innate and adaptive immune response end up working with each other right away to eliminate the pathogen.

In the primary immune response, naive B cells residing in the lymphoid follicles of the secondary lymphoid organs get activated through their interactions with other immune cells. First, macrophages trap antigens entering the lymphoid organs and take them to the follicles Here, the B cell acts as an antigen presenting cell - processing and serving up protein antigens to T follicular helper cells. In response, the T follicular helper cell expresses CD40L on its surface and produces IL-21, and together they induce the B cell to undergo class switching and affinity maturation. In class switching, the B cell shifts from expressing a B cell receptor with IgM and IgD to expressing IgG, IgE, or IgA. In affinity maturation, only the B-cells with a higher affinity to the specific antigen thrive as they can bind to even low levels of the antigen and still be stimulated to survive and differentiate.

Key Takeaways

B and T cells are the two main types of lymphocytes or white blood cells that play a role in the immune response. Both B and T cells can remember previous encounters with foreign antigens, which helps them to quickly and effectively respond to future infections by the same microorganisms.

B cells produce antibodies, which bind to pathogens and mark them for destruction by other immune cells. T cells kill infected host cells or help B cells produce more antibodies. Memory B and T cells persist in the body for many years, providing lifelong protection against reinfection by the same pathogen.