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Jackofknives
Cuddle bear inside  Topics: 101 Posts: 890 |
A 10-month-old infant girl is admitted to the hospital with signs of Pneumocystis cariii pneumonia. Studies of her peripheral blood demonstrate age-normal counts of CD19+ cells, but CD3+ and CD4+ cell numbers are depressed. Immunoelectrophoresis of her serum reveals a moderate hypogammaglobulinemia. Her peripheral blood lymphocytes proliferate normaly in response to phytohemagglutinin and MHC class I mismatched allogeneic cells. In a one-way mixed lymphocyte reaction using her cells as the stimulator cells, allogeneic T lymphocytes did not proliferate. Whic of the following best describes the molecule most likely lacking from her lymphocytes? A) It is designed to bind endogenously produced peptides B) It is designed to bind exogenously processed peptides C) It possesses Beta-2 microglobulin D) It possesses two chains of unequal length E) It should be present on all nucleated cells in the body I need an explanation for this one.
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SILVER
| DoWhatYouGotToDo!  Topics: 56 Posts: 1289
B) It is designed to bind exogenously processed peptides
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NNL
| Awaitin The Unexpected  Topics: 779 Posts: 6613
B) It is designed to bind exogenously processed peptides
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doc179
| Forum Guru Topics: 67 Posts: 1213
ok, I am also going for B, I dont think I have a logical explanation for this. I have been thinking why and the explanations I came up with are not satisfactory enough for me. But I opted for B by exclusion, all the other choices are related to CD8 and MHC1 since the CD4s are deficient I chose B. Pls let us know what the correct answer is and the right explanation. Thanx
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unique1
| __________  Topics: 16 Posts: 1964
I also choose B. Not sure if it is what I think though  . I think the molecule lacking from her lymphocytes are CD28 because T cells require two signals for complete activation. Signal 1 is provided by engagement of TCR by the appropriate MHC-peptide antigen complex and signal 2 is delivered by the interaction of CD28 molecules on T cells with costimulatory B7 molecules on the APCs. CD28 costimulation is critical , because in the absence of signal 2 the T cells undergo apoptosis or become unreactive(anergic).Please correct me if I am wrong.
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usmlefever
| Forum Senior Topics: 4 Posts: 125
CD4 is lacking which works via MHC2 & choice B is the characteristic oc MHC2 all other choices are representing MHC1 mol.choice D is wrong b/c MHC2 has 2 chains of equal size.
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jole
| Forum Newbie Topics: 39 Posts: 498
B
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Jackofknives
| Cuddle bear inside Topics: 101 Posts: 890
Yea B is listed as correct answer "Her peripheral blood lymphocytes proliferate normaly in response to phytohemagglutinin and MHC class I mismatched allogeneic cells. In a one-way mixed lymphocyte reaction using her cells as the stimulator cells, allogeneic T lymphocytes did not proliferate." What about here? How does lacking of MHC2 help with proliferation in allogeneic cells considering you still have a set of MHC1s?
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acintya
| Power to Choose...  Topics: 7 Posts: 759
Here is my understanding... because she still has MHC1s, she can still recognize other cells as foreign and proliferate in response to phytohemagglutinin, but because her cells do not express MHC2, her cells cannot be recognized by allogeneic cells.... and hence no proliferation in response to allogeneic T lymphocytes. ????
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godfather1212m
| Forum Guru  Topics: 44 Posts: 476
this is a case of bare lymphocyte syndrome. where MHC II molecules are deficient as you know they are the ones resposible with dealing with exogenous peptides. so choice B is the only to be correct
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Jackofknives
| Cuddle bear inside Topics: 101 Posts: 890
MCH class I allotypes can be recognized by NK classes, a mismatch will release the inhibitory input and render them active, not talking about the cells mostly responsible for rejection - CTL also recognize MCH class I mismatches. Also MCH class I is expressed in all nucleated cells, which makes this more perfuliar. Thats why this seem very confusing. bare lymphocyte syndrome is not restricted to MCH class II, another form is mutation in TAP complex resulting in no peptides enter then ER and therefore peptides cannot bind MCH class I and MCH class I on the cell surfaces is greatly diminished. so bare lymphocyte syndrome is not only restricted to MCH class I. (my source is: Parham P80)
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