B5- Cell Recognition and The Immune System Flashcards
What is an antigen?
- Foreign molecule / protein/ glycoprotein / glycolipid
- That stimulates animmune responseleading to production ofantibody
How are cells identified by the immune system?
- Each type of cell hasspecific moleculeson itssurface(cell-surface membrane / cell wall) that identify it
- Oftenproteins→have aspecific tertiary structure(or glycoproteins / glycolipids)
Antigen Variability
- Some pathogens exhibit antigen variability:
- Antigens on their surface change frequently due to mutations
- Results in new strains of the pathogen
- Consequences of antigen variability:
- The specific immune response becomes ineffective
- Antibodies from lymphocytes and memory cells can no longer bind to the altered antigen
- Pathogen can evade recognition by the immune system
What types of cells and molecules can the immune system identify?
- Pathogens(disease causing microorganisms) eg. viruses, fungi, bacteria
- Cells from other organismsof the same species (eg. organ transplants)
- Abnormal body cellseg. tumor cells or virus-infected cells
- Toxins(poisons) released by some bacteria
Describe phagocytosis of pathogens (non-specific immune response)
Phagocytes attracted by chemicals/ recognises antigens on pathogen
Phagocyte engulfs pathogen by surrounding it with its cell membrane
Pathogen contained in vesicles
Lysosome fuses with phagosome and releases lysozymes
Lysozymes hydrolyses pathogen
What does phagocytosis lead to?
Phagocytosis leads topresentation of antigenswhere antigens are displayed on the phagocytecell-surface membrane, stimulating thespecificimmune response (cellular and humoral response).
Describe the response of T lymphocytes to a foreign antigen (the cellular response)
B lymphocytes can recognisefreeantigens eg. in blood or tissues, not just antigen presenting cells.
Specifichelper T cells with complementary receptors(on cell surface) bind to antigen onantigen-presenting cell→activated and divide by mitosis to form clones whichstimulate:
- Cytotoxic T cells→kill infected cells / tumour cells (by producing perforin)
- Phagocytes→engulf pathogens by phagocytosis
Describe the response of B lymphocytes to a foreign antigen (the humoral response)
1.Clonal selection:
- Specific B lymphocytewithcomplementary receptor(antibody on cell surface) binds toantigen
- This is then stimulated byhelper T cells(which releases cytokines)
- So divides (rapidly) bymitosisto formclones
- Some differentiate intoB plasma cells→secrete large amounts of (monoclonal)antibody
- Some differentiate intoB memory cells→remain in blood for secondary immune response
What are antibodies?
- Quaternary structure proteins(4 polypeptide chains)
- Secreted byB lymphocyteseg. plasma cells in response tospecificantigens
- Bindspecificallyto antigens formingantigen-antibody complexes
Explain how antibodies lead to the destruction of pathogens
Antibodiesbind to antigenson pathogens forming anantigen-antibody complex
○Specifictertiary structuresobinding site / variable region bindstocomplementary antigen
- Each antibody binds to2 pathogensat a time causingagglutination(clumping) of pathogens
- Antibodiesattract phagocytes
- Phagocytes bind to the antibodies andphagocytose many pathogens at once
Explain the differences between the primary & secondary immune response
- Primaryfirst exposure to antigen
- Antibodies producedslowly& at alower conc.
- Takes time for specificB plasma cellsto be stimulated to produce specific antibodies
- Memory cells produced
- Secondarysecond exposure to antigen
- Antibodies producedfaster& at ahigher conc.
- B memory cellsrapidly undergo mitosis to produce manyplasma cellswhich produce specific antibodies
What is a vaccine?
- Injection ofantigensfromattenuated(dead or weakened) pathogens
- Stimulating formation ofmemory cells
Explain how vaccines provide protection to individuals against disease
- SpecificB lymphocytewith complementary receptor binds toantigen
- SpecificT helper cellbinds toantigen-presentingcell andstimulatesB cell
- B lymphocyte divides bymitosisto form clones
- Some differentiate intoB plasma cellswhich releaseantibodies
- Some differentiate intoB memory cells
- Onsecondary exposureto antigen,B memory cellsrapidly divide by mitosis to produceB plasma cells
- These releaseantibodies fasterand at ahigher concentration
Explain how vaccines provide protections for populations against disease
Herd immunity-large proportionof population vaccinated, reducingspreadof pathogen
- Large proportion of populationimmunesodo not become illfrom infection
- Fewer infectedpeople to passpathogenon /unvaccinatedpeopleless likelyto come incontact with someone with disease
Describe the differences between active and passive immunity
No exposure in passive so no memory cells given from another organism so faster acting as specific but short term
Active has to have initial exposure so memory cells created produced by b plasma cells so takes longer to develop giving long term immunity.
Explain the effect of antigen variability on disease and disease prevention
- Antigens on pathogenschange shape / tertiary structuredue togene mutations(creating new strains)
- Sono longer immune(from vaccine or prior infection)
- B memory cellreceptors cannot bind to / recognise changed antigen on secondary exposure
- Specific antibodiesnot complementary / cannot bindto changed antigen
Describe the structure of a HIV particle
Lipid envelope, RNA, Reverse Transcriptase, Capsid and Attachment Proteins
Describe the replication of HIV in helper T cells
- HIV attachment proteinsattach toreceptorsonhelper T cell
- Lipid envelope fuseswith cell-surface membrane, releasingcapsidinto cell
- Capsid uncoats,releasing RNAandreverse transcriptase
- Reverse transcriptaseconverts viralRNA to DNA
- Viral DNAinserted / incorporatedinto helper T cellDNA(may remain latent)
- Viral protein / capsid / enzymesare produced
- DNAtranscribedinto HIV mRNA
- HIV mRNAtranslatedinto new HIV proteins
- Virus particlesassembledandreleasedfrom cell (via budding)
Explain how HIV causes the symptoms of acquired immune deficiency syndrome (AIDS)
- HIV infects andkills helper T cells(host cell) as it multiplies rapidly
- So T helper cells can’t stimulatecytotoxic T cells,B cellsandphagocytes
- So B plasma cells can’t release as manyantibodiesfor agglutination & destruction of pathogens
- Immune system deteriorates→more susceptible to (opportunistic) infections
- Pathogens reproduce, release toxins and damage cells
Explain why antibiotics are ineffective against viruses
- Viruses do not havemetabolic processes(eg. do not make protein) /ribosomes
- Viruses do not havebacterial enzymes / murein cell wall
What is a monoclonal antibody?
- Antibody produced fromgenetically identical / cloned B lymphocytes / plasma cells
- So havesame tertiary structure
