Microbiology Questions that confuse me

[Tonino]

Hey guys I'm a microbiology major. I know some of these questions are a bit out of scope for the MCAT but I feel like I would be that much more confident going into my test in January. I hear that there's a big portion of microbiology in the biology section so I feel this will help tremendously. Thanks for reading!

1. MHC and Transplant Rejections
I'm just wondering why MHCI specifically would be involved in allograft rejections... such as a kidney.

My understanding is that since MHCI is found on all nucleated cells, it would be quite prevalent throughout the human body system, therefore easily detecting any foreign molecule.

Then how would MHCII be involved in transplant rejections as well?

2. B220 on B cells = CD45R
B220 is a surface marker on B cells.

B220 is rather another name for CD45R, the ligand which is present on helper T cells that binds to CD22 on APC to activate T helper cells by cleaving phosphates off certain signalling molecules of the CD3 apparatus.

This being so, does it not mean that B cells binds to APC? This confused me, as I knew of B cell – T helper cells interaction, but not the former.
B cell itself is an APC, so it further does not make sense.

3. MHC, the peptide, and TcR. The trio.
a. MHC molecule (alpha and beta chains) are held together by non-covalent interactions.

b. Is the peptide held on the hypervariable region of the MHC molecule by non-covalent interactions as well?

c. when the TcR binds to the peptide on the MHC and to the MHC itself, are they also non-covalent interactions?

4. Infectious Mononucleosis
I was wondering why a disease that causes mononucleosis is associated with polyclonal activation?

Isn’t mononucleosis just a rise in the number of monocytes in the blood? B cells are the ones responsible for polyclonal activation, so why are they involved in this scenario?


if you just answer the question in reference to their number, that would be of great help. Thanks guys!

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[MLT2MT2DO]

Ok well 1-3 are either over my head or it has been a couple years since I went through the material (depending on which number).

4. I can answer easily as many older physician's today make the same honest mistake as yours.

In short Mono is not an increase of monocytic cells, it is actually an increase in atypical lymphocytes (B lymphocytes).

When mono was first described it was also thought that it was an increase in monocytes since little were known about the existence atypical/variant lymphocytes. The name has since stuck with the disease though the cause has indeed been found to be atypical lymphocytes.

If you look at these two cells on a slide they share similar traits, though you will notice atypical lymphs don't have vacoules and they have a much darker cytoplasm which extends towards the red cells.

 

[BennieBlanco]

Hey guys I'm a microbiology major. I know some of these questions are a bit out of scope for the MCAT but I feel like I would be that much more confident going into my test in January. I hear that there's a big portion of microbiology in the biology section so I feel this will help tremendously. Thanks for reading!

1. MHC and Transplant Rejections
I'm just wondering why MHCI specifically would be involved in allograft rejections... such as a kidney.

My understanding is that since MHCI is found on all nucleated cells, it would be quite prevalent throughout the human body system, therefore easily detecting any foreign molecule.

Then how would MHCII be involved in transplant rejections as well?

2. B220 on B cells = CD45R
B220 is a surface marker on B cells.

B220 is rather another name for CD45R, the ligand which is present on helper T cells that binds to CD22 on APC to activate T helper cells by cleaving phosphates off certain signalling molecules of the CD3 apparatus.

This being so, does it not mean that B cells binds to APC? This confused me, as I knew of B cell – T helper cells interaction, but not the former.
B cell itself is an APC, so it further does not make sense.

3. MHC, the peptide, and TcR. The trio.
a. MHC molecule (alpha and beta chains) are held together by non-covalent interactions.

b. Is the peptide held on the hypervariable region of the MHC molecule by non-covalent interactions as well?

c. when the TcR binds to the peptide on the MHC and to the MHC itself, are they also non-covalent interactions?

4. Infectious Mononucleosis
I was wondering why a disease that causes mononucleosis is associated with polyclonal activation?

Isn’t mononucleosis just a rise in the number of monocytes in the blood? B cells are the ones responsible for polyclonal activation, so why are they involved in this scenario?


if you just answer the question in reference to their number, that would be of great help. Thanks guys!

0 chance these are MCAT related.

 

[Aphtalyfe]

1. MHC and Transplant Rejections
Then how would MHCII be involved in transplant rejections as well?

2. B220 on B cells = CD45R
B220 is a surface marker on B cells.

B220 is rather another name for CD45R, the ligand which is present on helper T cells that binds to CD22 on APC to activate T helper cells by cleaving phosphates off certain signalling molecules of the CD3 apparatus.

This being so, does it not mean that B cells binds to APC? This confused me, as I knew of B cell – T helper cells interaction, but not the former.
B cell itself is an APC, so it further does not make sense.

3. MHC, the peptide, and TcR. The trio.
a. MHC molecule (alpha and beta chains) are held together by non-covalent interactions.

b. Is the peptide held on the hypervariable region of the MHC molecule by non-covalent interactions as well?

c. when the TcR binds to the peptide on the MHC and to the MHC itself, are they also non-covalent interactions?

1. MHCII can be involved in graft rejections in multiple ways... I'll just briefly explain one such possibility... since like others have said... this is WAYYYY beyond the scope of the MCAT.

One way is that T-cells (helper) contained within the graft are activated via recognizing the recipient's dendritic cells. The mechanism is a little deep but just know that donor T-helper cell TCR binds to MHC class 2 subunits on recipient dendritic cells (a type of APC) and are activated without actually having to recognize a presented peptide. (form of graft vs host disease)


2. Even in medical immunology we barely discussed CD45... I wouldn't worry about it for the MCAT. Maybe by the time you take the class they will have more conclusive information about it?

3. I believe all bonds that you mentioned are non-covalent.

4. The above poster already answered this one.

All your questions are FAR deeper than the scope of the MCAT... but I know how it feels to have burning questions even if they are completely non-relevant to the short-term.

Good Luck