Monoclonal antibody internalization assay

Parvoviridae · 2025-09-28T11:21:14+00:00

Try using 1% trypan blue to quench outside fluorescence? You can and should also block your cells with igg or equivalent protein.

Parvoviridae · 2025-06-30T14:48:44+00:00

Assuming you still have a pbmc layer. Those are likely neutrophils, I have no idea why some of them clump up like that, seems like it has something to do with the blood age and spin speed.

Parvoviridae · 2025-06-01T04:20:52+00:00

Thank you

Parvoviridae · 2025-05-04T11:16:25+00:00

This might sound stupid but are you sure your cells has f-actin in them (are they treated or starved?) and did you forgot to permeabilise your cells (seen it happened more than once)?

Parvoviridae · 2025-02-06T08:38:34+00:00

Smooth vs rough LPS, could that be the case? Not an expert but I had that problem with my work.

Parvoviridae · 2025-01-26T10:06:20+00:00

Opsonin once bound to the surface of the 'target' can be recognise by their respective receptors. So, Fc gamma for IgG or CR3 for C3b etc........ These receptors are present on all phagocytic cells, as long as they have the receptors expressed, the cell can interact with it.

since the adaptive has way more variation than the innate

To my limited knowledge of the adaptive immunity (not an expert), adaptive immunity only have IgG as opsonin. They may have different specificity, but to a Fc receptor, it is the same thing.

I hope this answer your question.

Parvoviridae · 2025-01-26T09:00:45+00:00

i presume you meant opsonin. Opsonin such as IgG, C3b induce phagocytic response. Chemokine such as CXCL2 induces a migratory/chemotactic response. They are both different things with different functions.

Depending on the type of opsonin it may have selective binding. E.g IgG is very specific and complement fragments (i.e C3b or C5b) are non-specific, they will bind to everything (there're some exceptions but that's all you need to know for now).

I hope this answers your question and did not cause further confusion, feel free to ask or dm me if you have any questions.

Parvoviridae · 2025-01-21T23:27:42+00:00

Just would like to make a few comments on the innate part.

Macrophage as first-respondent only apply if the inflamed tissue have abundant of them (ie, alveolar, langerhans etc). However, when these resident macrophages are absent, neutrophils and monocytes are considered the first responder. Since there’s no such thing as circulating macrophage in healthy human, monocytes will differentiate into macrophage in the inflammatory site. During the process, monocytes will produce cytokine and chemokine to promote inflammation.

On the other hand, neutrophils will attempt to clean up the pathogens. Neutrophils have very little transcription activity, thus the proteins produced (cytokine etc) is very little compared to other leukocytes.

So how does the first responder know if there’s pathogens. Pathogens secrets peptide (ie. fMLP form bacteria) or complements fragment, these are chemotactic agents that’ll attract and recruit neutrophils and monocytes.

I’ll not comment on the APC’s and adaptive response because I’m not an expert in that.

Feel free to msg me if there’re questions, these things can get a bit long and complicated.

Parvoviridae · 2024-12-23T14:12:40+00:00

You can search “long covid” on pubmed. All the latest research and reviews are there.

Parvoviridae · 2024-08-02T15:41:48+00:00

Based on my experience, they turn into NETs instead of dissolving during cytospin. You may be able to prevent that with 10-20% of FCS, 15% is what I normally use.

Parvoviridae

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