Hi, i am a med student and i was given a mock case study to work on... there is a 38yrs old patient who presents with maculopapular rash all over her body after 6 days of taking betalactames for tonsillitis. She didn't have any respiratory symptoms nor GI problems. Which would suggest some milder delayed hypersensitivity reaction. But then my supervisor gave me "test results" which showed elevated IgE specific for betalactames and also positive basophilic activation test, both of these test being positive in type 1 hypersensitivity. So my question is - is it rather some weird IgE mediated reaction, or is it possible that the patient would have type 4 reaction and later on IgE senzitization would happen?

Hello,

I'm taking an immunology course and find myself confused by a certain question presented by our professor. She asked the following question:

Which immune system receptors recognize PAMPs such as LPS or flagellin?

a. Only innate immune system receptors

b. Only adaptive immune system receptors

c. Both innate and adaptive immune system receptors

I thought the answer would've been A, but she's persistent and says that isn't true, and the correct answer is C. Everything I searched online is saying the answer should be A because the innate cell receptors are the ones that recognize PAMPs. If someone could provide clarification on the answer and the explanation, that would be appreciated.

Hi all,

I am a MSc Immunology student at Imperial College London, and am starting to apply to a few graduate schemes and jobs in pharma companies.

I have received a few rejections already and I cant seem to understand why. I also would like to hear from people who are in the industry some advice or tips.

I m really struggling and confused since I assumed my CV was quite strong. Should I start applying for internships instead and then try to get a full time?

Hello all,

I am struggling to understand the difference between an opsin and a chemokine. From my understanding a chemokine is a chemical messenger that attracts leukocytes to the site of an infection, but an opsin is a protein that physically "tags" (binds to) a pathogen and facilitates phagocytosis through binding interactions between the leukocyte and the pathogen. Are opsins a type of a chemokine or are they their own classification of molecule? Also, because opsins work on the basis of physically enhancing the binding of a leukocyte to a pathogen, thus enhancing phagocytosis, are opsins only effective on pathogens that have specific receptors for the opsin to bind to?

I'm sorry for the questions, been reading about this for awhile now and the textbook I'm using is vague and doesn't go super in detail on the specific molecules involved with the innate system.

I live with family who are heavily immune compromised and the norovirus outbreak has been scary me so much bc there’s so many different strains you can never even get immunity from it. I ordered some hibacleanse from Amazon bc I recently found out that antibacterial soaps don’t kill viruses (shocker, not really but I was dumb and didn’t put two and two together)

After ordering it though, I discovered that apparently it can cause superbugs to develop, I know antibiotic resistant bacteria is on the rise but at the same time I’ve had so many rounds of antibiotics that I didn’t need throughout my life I’m more concered about that then I am about what a more advanced soap could do. However, I still want to be educated. What are the odds of using antimicrobial soap being harmful and increasing the risk of bacteria mutations, etc? Is it okay if you only use it during flu season?

Hi, I am a peds resident in big academic center. I am interested in Allergy&Immunology or Rheumatology for fellowship. I am also very interested in basic/translational research. My main interest is in innate immunity and immune dysregulation syndromes especially auto inflammatory syndromes like recurrent fevers, HLH, MAS as well as defects in innate immunity. I am interested in studying inflammasome activation and caspase pathways. Which fellowship would fit better to me?

Hi does anyone have any good uni recommendations for immunology degrees in england? Or any that I can get a related degree in the field?

I will be clear from the beginning, this interest and curiosity was born out of a medical concern, but all of that is being handled by my doctor, a specialist, and labs. I no longer have questions related to my situation. :) I have been interested in vaccines since around 2018, and wow did the next few years give me some great, easy to find info!

I'm curious, is there such a thing as a non-responder to vaccines in general? And would it include all vaccines? Would that be impossible for some to be included? I don't know enough (thank you neuro + psych) about the different pathways and attack methods each use to know if some work in such a spectacularly different way that no one would be able to say they are a non-responder for ALL vaccines, all types.

Please share if you have a good book recommendation for learning more about the different versions of vaccines in a comparative way! I would love that.

• Inactivated vaccines
• Live-attenuated vaccines
• Messenger RNA (mRNA) vaccines
• Subunit, recombinant, polysaccharide, and conjugate vaccines
• Toxoid vaccines
• Viral vector vaccines

For my situation, it ended up being a ton of different scenarios that overlapped, like with most medical situations. :) They're still not totally sure about the answer, but the important thing I took away were the instructions to make sure I'm properly vaccinated and up to date. :)

If you have cool videos a la Crash Course style, I would love to see those, too. Textbooks are fine with me. I enjoyed my nuero classes and pharmacology classes, and I think this would be the same kind of fun. I also have a friend that works in vaccines, so we could finally have some more in-depth conversations if I started to understand better. :) New interest loading. :)

Is anyone going to Immunology 2025 in Honolulu?

I'm thinking about attending and am curious about the vibe of the conference. I'm really focused on publishing scientific research and want to know if this is a good conference of people who do that.

TIA

Hello everyone. I’m working on a research project for my senior year of high school, and I am having trouble finding an answer online for some of my questions. My research project is looking at CD-19 production, but due to the constraints of cost and the laboratory quality I am unable to use B-Cells. I came across Hybridoma cells, and I was wondering if they are something that could be substituted for B-Cells in experimentation. I found one research paper that wasn’t very recent, but said that most Hybridomas still express CD-19 after fusion. Would this be a viable substitute for B-Cells? Thank you.

Can somebody explain to the bachelor student what is the difference between cytokine binding proteins and viroceptors? it seems that both of them prevent binding to cytokine receptors and alter the immune response, also both are encoded by viruses

I might be lost in my notes or maybe they are just wrong

I graduated just under a year ago with my Bachelors in Biology and a minor in Microbiology (I was one credit away from my minor - thanks to my advisor screwing me - and I need to wait until I have the money to finish that last credit).

This last summer I moved to Los Angeles hoping for more career choices. I am planning on getting a PhD in Immunology and Infectious Disease but I know thanks to my average GPA from my bachelors that I'll need to boost my application. I was planning on getting research experience (and ideally being included on a publication) during a gap period. Since I've moved I've filled out dozens and dozens of applications to research labs at places such as UCLA Health, USC, and Cedars-Sinai. Even borderline janitorial positions. I know these are more prestigious institutions, but I'm unsure of what else is in the area. I've looked at private sector, but there isn't much entry level work.

I have yet to hear back about a single application. I have gone over my resume, CV, and cover letters I submit so many times looking for ways to improve them. I have next to no experience outside of the lab experience from classes. I am frankly going crazy being unemployed and I'm losing hope. If anyone has advice on how to get an entry level research position anywhere in LA I would be grateful. I'm not entirely certain on what I want my immunology focus to be, but I'm leaning towards a focus on vector-borne disease (Malaria, Dengue fever, etc.). I am a very hard worker and I just need a chance to prove myself.

Does anyone have advice on how to get an entry level research position here in LA?

I need help analyzing this paper: https://www.nature.com/articles/ni.2606 . I get the gist of it, but I need to be able to "analyze the results" and present them as part of a journal club presentation, along with critiquing the paper for what they did well, what they could have done better, and creating an experiment that builds on this research. It's a 4th year course.

I'm returning to school after a year and I feel like I have forgotten everything and feel very dumb. I need all the help I can get. I have a rough draft of a script written that highlights the main points I would like to discuss. If someone could hop on Zoom with me for an hour and answer my questions about the paper and maybe look over the script that would be great 🤣 I am obviously willing to pay, but I am a broke uni student so it will not be much and it will be in CAD.

Please help me out. PLEASE !!!!!!!!

hi everyone! wondering if anyone can clear these concepts up for me:

1. so neutrophils are the first responders to a foreign pathogen. if they are not able to kill the pathogen, is that when they start recruiting other innate cells to help out? like macrophages, dendritic cells, NK cells, etc? And they do this by producing cytokines or how?

2. Transitioning from innate --> adaptive response, APCs will present the antigen to B lymphocytes first or what is the order? I'm just getting really confused on the timeline of things. In my lecture, it is said that antigen bound to a BCR is internalized and then presented to MHC class II. Does the b lymphocyte have the ability to bind to an antigen without the help of the innate cells?

3. the next part of my lecture says that b lymphocytes presents to CD4+ t lymphocytes which allows t cell to help b cells to produce high affinity antibodies. So the order is BCR presents antigen to Helper T-cell -> Helper T-cell goes back to b cell to tell it what to produce in terms of antibodies? Why wouldn't APCs like DCs just go straight to b-cell to create the antibody? do they just not have the receptors for it?

sorry for the long post, and thank you in advance for any clarification that you can provide. :D

I’m an adult but I didn’t finish high school and biology has been rough for me as it is. I’m in the process of getting my GED but also taking some spare time to learn about the immune system and infectious diseases as it’s something I’m really interested in and want to study. I know Coursera isn’t an official thing and it won’t help you get into college or anything but I was just wondering if there are any courses on there that could be helpful for learning the basics as someone who’s new to immunology?

Hi,

I'm trying to run a Treg suppression assay on Tregs isolated from frozen pt PBMCs. We sort both Treg (CD3+ CD4+ CD25hi CD127lo) and Tcon (CD3+ CD4+ CD25lo) populations and co-culture with CFSE labeled Tcons from a healthy donor. When we look at these samples on flow, we see suppression in the Treg/Tcon co-culture, but we also see suppression in the Tcon/Tcon co-culture. Has anyone else run into this issue and knows what is going on? Thanks!

Hiii does anyone know an affordable immunotherapy for metastatic pulmonary adenocarcinoma? Cuz chemo and radiotherapy sucks

Hi! I am writing a near-future sci-fi novel, wherein a world power has engineered a virus as a last gamble to sway a war in their favor. This hypothetical virus would, if there is any sensible way for it to conceivably be done, target young people of working age more than any other age range, and perhaps even men disproportionately more than women. This way, they'd reason, it would cause military efforts in a nation infected with it to crumble, but without it being a risk so huge it would be likely to cause the downfall of the very world power spreading this virus. They would take as many preventative measures as possible, and carefully spread it in strategic locations.
For extra context, ideally, it would be something that can linger, and spread through aerial means at short distances, unless it encounters extreme temperatures or the like.

If there are ways to accomplish this, for example with a viral carrier specifically engineered to discern environmental factors, or through extremely specific genetic engineering of the virus itself, or anything else you can think of, do let me know. And feel very welcome and encouraged to speculate about any related topics, I am always eager to expand my purview and change any plot elements to reflect that. Thank you!

I’m a third year undergrad and I’ve been accepted into two labs as a research assistant and am having trouble deciding which one to go with.

One of them works with methane-consuming microbes (mostly bacteria and archaea) and I’ll mostly be doing DNA sequencing and some statistical analysis.

The other works with mammalian cells and how they react to their environments and I’ll be doing cell culture and maybe some analysis as well.

Are either of these more relevant to an industry job than the other or does it not matter as much as long as I am getting some experience outside of classes? I’m equally interested in both labs so that isn’t a concern.

In this interview, Paul Offit, infectious disease expert, said that there has never been an example in history of a vaccine whose severe side effects are delayed by years. He says the severe side effects of any vaccine is always within a few weeks.

Question at about 51:22 of the video below. https://www.youtube.com/watch?v=A27ameSqcQs

Is this correct?

Long shot- does anyone have an example of a funded k22 that's immuno based that you'd be willing to redact identifiable info out of and share with me, I'm writing one and I'm trying to see every funded example possible! I have looked at NIAID samples but there's only one k and it's really not immuno adjacent at all....thx friends!

is there any literature close to the subject?

Hello! I am a very recent graduate, and I was looking to apply for a medical laboratory science program. Unfortunately, during my undergrad, I was not aware of this program until I was close to graduating, and as a result am missing a single immunology course that is required in order to apply. I was told I could try UC Berkely, but their courses are in the $1300K range, which isn't really affordable for me, especially since I don't know if it's even certain I'll be able to get into the MLS program if they are competitive. I don't suppose anyone has any other resources for other possible online programs that are accredited and can transfer?

Thank you very much!

Fellow academic here. Recently tried to run an experiment where we isolate CD8+ T cells from one mouse strain and adoptively transfer them into mice of another strain. We took 8 mice (aged 8 weeks), isolated ~600 million splenocytes and used a commercially available CD8+ T cell enrichment kit to get ~45 million CD8+ T cells. I then stained them using CellTrace Violet according to the manufacturer (I have been using it this way for three years now, just not this many cells - usually 8-10 million) by using 1ul/1mL/1 million cells - ie: 45 uL of CellTrace into 45mL containing 45 million cells. After 20 minutes of staining I washed twice with PBS, resuspended and counted. I ended up with 12 million cells, not enough to do the adoptive transfer. From reading and consulting with other researchers, I either overlabeled the cells or aspirated the pellet at some point. I am leaning towards the former as a colleague uses this same CellTrace Violet but at 0.5 uL/1mL/20 million cells - meaning I could have (very much) overlabeled them and thus caused this massive loss as we know there is some loss with this dye. Usually I see about 1-2million cells lost. When running this experiment last time, we went from 54 million CD8+ T cells to 20 million, which is why I think I just overlabeled and killed them all. Theoretically I could have aspirated the pellet but I have been doing this splenocyte isolation with CD8+ T cells and CellTrace for years without aspirating the pellet. Any thoughts?

Thanks in advance from a researcher needing more coffee.

I see plenty of info regarding becoming a clinical Immunologist, but nothing on those who don't want to work with patients, only in research which is what I want. So I was curious to see if anyone here knew anything about what direction I should take to do that?? TIA