10) mucus pretty much just traps the microbial and and allows your cell-mediated response to kick in, and it's found pretty much in your respiratory tract and digestive tract and your reproductive tract. Mucus also contains digestive enzymes in it to fight microbes. it also contains dimeric IgA in it which you could write if depending on how your professor views "nonspecific antimicrobial effects"
low ph is found in the stomach, inside some cells like the granules of neutrophils, and even your skin. it pretty much provides an environment that is too harsh for the microbial to live in. it can also activate certain digestive enzymes and zymogens to digest the microbe.
lysozymes (which is also found in mucus), like cialda stated, disrupts bacterial cell wall integrity.
11) lots of B and T cells are made everyday. B cell development begins in the bone marrow where it'll undergo somatic mutation to develop a hypervariable domain that is specific for one type of antigen. before leaving the bone marrow, the B cell will undergo negative selection to get rid of the B cells with receptors that bind to self-antigen (aka autoreactive B cells). Once they leave the bone marrow, the naive, but mature B cell will travel and hopefully be recruited into secondary lymphoid organs. Inside the 2ndry lymphoid organs, if it binds to an antigen on it's b cell receptor, endocytoses the receptor and then expresses it on MHC I or II. This B cell will now be a professional antigen presenting cell and may form cognate interactions with a T lymphocyte that has survived positive and negative selection inside of the thymus to form a germinal center reaction and produce clones of itself. some of these progenies will become plasma cells like cialda stated, however, they'll only secrete only IgM since i'm going to assume that this is a primary infection. The rest of the progenies will undergo affinity maturation through somatic hypermutation and isotype switching through the expression of AID and generate new B cell receptors. These progenies will new receptors will compete with one another for a survival signal from the T cells (non-memory B cells do not survive very long). Of course, the progenies with receptors with higher affinity than the parent B cell will be "selected for" aka the clonal theory of selection.
tl:dr, you pretty much keep generating new B cells different B cell receptors. through somatic hypermutation and affinity maturation, you'll be able to generate and keep the ones with better affinity than what you started with, but you'll also weed out the ones that are autoreactive (aka fail negative selection at primary lymphoid organs)
12) pretty much what cialda said. ultimately, during a secondary immune response (which is how a vaccine works), you would've already had developed a B cell with a high affinity B cell receptor and a constant domain that isn't IgM whose progenies would've become a memory cell that circulates in your bodies or lining certain areas of your body such that when you become infected again, the memory cell will replicate and provide plasma cells that secrete the high affinity immunoglobulin right away. I forgot to mention before that developing this high affinity B cell receptor takes weeks to complete, so during a secondary immune response, you'll react a lot faster to the pathogen.