Granulocyte

 A granulocyte is a type of cell, so the correct category is:

✅ Cellular defense

Explanation:

Granulocytes are white blood cells that help fight infection. They are part of the innate immune system and include:

• Neutrophils – attack bacteria
• Eosinophils – fight parasites
• Basophils – involved in allergic reactions

Since they are actual cells that act in defense, they fall under cellular rather than physical (like skin) or chemical (like stomach acid or lysozyme) barriers.

 During antibody-mediated opsonization, phagocytic cells (like macrophages and neutrophils) bind to the Fc region of the antibody. This Fc region is the constant part of the antibody that sticks out after the Fab (antigen-binding) regions attach to the target (like a bacterium). Phagocytes have Fc receptors that specifically recognize and bind to this Fc portion, leading to phagocytosis of the tagged pathogen.

• Fc = "Fragment crystallizable" region = site for phagocyte binding

• Fab = "Fragment antigen-binding" = binds the antigen

• Variable region = part of Fab that specifically recognizes the antigen

• Disulfide bonds = hold antibody chains together, not used for phagocyte binding

✅ Correct choice: Fc

Which of the following statements is true? Group of answer choices In the secondary response to an antigen, higher levels of IgM will be detected in an individual’s serum. In the secondary response to an antigen, lower levels of IgM will be detected in an individual’s serum. The lag period following secondary exposure to an antigen is longer than the lag period following primary exposure. The lag period following secondary exposure to an antigen is shorter than the lag period following primary exposure

The correct answer is: The lag period following secondary exposure to an antigen is shorter than the lag period following primary exposure

Explanation:

• In a primary immune response, the body takes time (longer lag period) to recognize the antigen and activate the immune system.

• In a secondary immune response, memory B cells and memory T cells respond much faster, resulting in a shorter lag period and a stronger antibody response, mostly IgG.

Let’s review the options:

• ❌ Higher levels of IgM in secondary response – False; IgG is dominant in secondary responses.

• ✅ Shorter lag period in secondary response – True

• ❌ Lower levels of IgM in secondary response – Misleading; IgM is still present, but not the main antibody.

• ❌ Lag period longer in secondary – False

✅ Correct choice: The lag period following secondary exposure to an antigen is shorter than the lag period following primary exposure

NK Cells

Type of immunity:

✅ Innate immunity

Subtypes:

✅ No well-defined subtypes (though there are functional differences, NK cells are not divided into CD4/CD8 like T cells)

Works on:

✅ Virus-infected cells and tumor cells

Function(s):

✅ Kills abnormal cells (such as virus-infected or cancer cells) using cytotoxic granules; also secretes cytokines like IFN-γ

Receptors that this cell "sees" to induce function:

✅ MHC I (absence or downregulation of MHC I activates NK cells)

NK cells use activating and inhibitory receptors to detect stress signals and low MHC I expression.

 

Antimicrobial Drugs Extra Resource for Lab

 

In lab, you were introduced to the concept of microbial control:  the strategies we use to keep pathogenic microbes from keeping us sick, or to eliminate those that are making us sick.  We discussed the fact that there are really two different facets to this conversation:  controlling microbes in the environment around us, and controlling the microbes that have made it into our bodies already.  

 

There are two general strategies for controlling pathogenic microbes in the environment (shown in green above)

• Physical Control Methods (i.e. temperature, UV light, radiation, filtration)
• Chemical Control Methods (i.e.  detergents and soaps, chemicals that alter the pH, alcohol, aldehydes) 

 

Analyzing physical and chemical methods to control microbial growth: There are lots of ways to control
microbes in the environment, but they all fall into four basic categories.

A. Decrease Cell Integrity: alterations in the cell walls or cell membranes to disrupt the integrity of the cell
B. Disrupt proteins: interfering with protein structures to disrupt metabolism and the way the cell functions.
C. Disrupt nucleic acids: interfering with nucleic acid structures interferes with protein production and reproduction
D. Degerming: removal of microbes from the surface or area

 

While these strategies are really useful in the environment, we cannot use disinfectants or harsh physical methods to eliminate pathogens inside the body as they are toxic to humans and may damage our tissues along with the infectious microbe. Instead, we use antimicrobial drugs (in red on the diagram above) to control different microbes including bacteria, fungi, parasites (protozoa and worms) and viruses.

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Antimicrobial Drugs

Most antimicrobial drugs work to control the growth of microbes by using one of the following strategies:

• Decrease cell integrity:  Agents that target the cell wall or plasma membrane
• Disrupt protein production:  Agents that affect the ability of the microbe to make proteins
• Disrupt genome production/expression:  Agents that target genome replication and transcription
• Disrupt attachment:  Agents that disrupt attachment of microbes from their target receptors
• Disrupt metabolism: Agents that disrupt energy production or the production of building blocks (i.e. amino acid production, nucleic acid production)
• Disrupt structure:  Agents that disrupt large scale structures (i.e. scolex, muscles in helminths)
• 
  

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Drug Design and Selection

When designing drugs or choosing the proper drug to prescribe, there are lots of considerations including:

1. Selective Toxicity:  the drug should be toxic to the microbe without being toxic to the host.  This is not to say that drugs that are toxic to the host are never used, it is just that they are used MUCH less often.  The risk of the infection would have to be greater than the risk of the toxic effects of the drug.  

 

2. Target of Treatment: the drug must act on a target that actually exists in the microbe.  For example, a drug that targets the bacterial ribosome is an excellent choice for treating a bacterial infection.  However, a drug that targets the bacterial ribosome is a poor choice for treating a virus (doesn't have a ribosome at all) or a fungi, protozoa or helminth infection (all contain eukaryotic ribosomes rather than bacterial ribosomes).

 

3. -cidal treatments vs. -static treatments:  A drug that kills the targeted microbe are considered -cidal drugs.  However, not all drugs kill the microbe they are targeting.  Some drugs inhibit the growth and reproduction of the targeted microbe.  These drugs are considered -static drugs.  Static drugs are used to restrict the growth and spread of the microbe.  

 

4. Spectrum of antimicrobial activity: the drugs that we use affect different populations of microbes.  There are drugs that affect bacteria, drugs that affect fungi, drugs that affect helminths, etc.  Even within these groups, there are drugs that affect only subsets of the group.  (see the figure below).  A drug that targets all or most of the microbes in a group (for example, tetracycline), is considered a broad spectrum antimicrobial.  One that is very specific for only a small subset of the microbes in a group are considered narrow spectrum antimicrobials (for example, penicillin).  The range of activity is determined by the target of the drug.  Tetracycline affects the ribosome, which all bacteria have and so it is broad spectrum.  Penicillin targets the peptidoglycan, which is only accessible in gram positive bacteria and is therefore a narrow spectrum drug.  Spectrum is determined within target microbe group. Even a broad spectrum antibiotic doesn’t target viruses or any of the eukaryotic pathogens. 

 

 

5. Drug Resistance:  We've talked about ways that antimicrobial resistance can emerge in a population of microbes (spontaneous or induced point mutations and horizontal gene transfer) and how exposure to antimicrobial drugs kills susceptible microbes and leaves behind a population of microbes that is resistant to the drugs. We've talked about how some viruses, especially, accumulate those mutations VERY quickly (think about HIV and SARS CoV-2) Today, we are going to think about impacts and complications that arise when microbes having or are able to attain that kind of drug resistance when we are thinking about how to help patients by prescribing them antimicrobial drugs.  

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A note on drugs & spectrum!!

Sometimes the theory of a drug is a bit different from the effect we observe in the lab. This can tell us important information about the chemical properties of specific drugs. Depending on the chemical properties of a drug, this can influence how the drug gets into organisms.

Take a note on aminoglycosides in the figure below. The uptake is mediated through pores present in the OM as illustrated. Although the target (bacterial ribosomes) would suggest a broad-spectrum effect, what class of bacteria would most likely be affected the most?

Previous

Next

 In this pre-class lecture, we'll be going over the physical and chemical barriers of innate immunity. In class on Monday, we'll learn more about the cellular components in detail.

 

After we finish on Monday, it might help you to take a look at this youtube video again (posted in your study guide) as well as other videos to really get the details solid in your brains before we move on to the adaptive immunity. 

 

MY BIGGEST advice with the immune system is review review review. Make sure you stay on top of your studying here because it is going to get really detailed really quicky. Most of it isn't super complicated like some of the other materials we have covered, but is a LOT of details that you need to keep organized in your brain and that's what makes it hard.

 

 HIV is RNA virus ,  ++SS RNA virus , the main enzyme reverse transcriptase. When copying make many mistakes when Copy RNA to DNA. 

The enzyme do not have proofreading function like human. 

This is why the mutation lead fast evolution. 

The drug target reverse transcriptase using NRTI drug (Nucleotide reverse transcriptase inhibitors).

 The drug blocks the virus from copy RNA to DNA 

The virus mutates often so the resistance can develop causing the drug stop working or not effecting.