FAQ
Q: Which Panel should I start selecting from?
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A: If you just want to quickly confirm "whether it is recognized by innate
immunity and triggers a response," it is recommended to start from PRR Trigger Standard Edition
(TNF-α + IL-6) Start; if your model is biased towards virus/nucleic acid stimulation, prioritize
from Type I Interferon Axis Standard Panel (IFN-β + CXCL10) Start. Once the direction is
confirmed, we will upgrade to the enhanced version for mechanism layering.
Q: For stimuli such as LPS/Poly(I: C)/CpG, which indicators are more suitable to observe
respectively?
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A:
- LPS (TLR4): More inclined towards the pro-inflammatory axis, often
prioritizing TNF-α, IL-6, (enhanced version includes IL-1β/IL-10).
- Poly(I: C) (related to TLR3/MDA5): More inclined towards the antiviral
axis, prioritize IFN-β and CXCL10 (IFN-α can be added).
- CpG (TLR9): Common pro-inflammatory + immune bias effects, prioritize
TNF-α, IL-6, and optionally include IL-12/IL-10 (for functional stratification).
Q: Why do I detect an increase in TNF-α/IL-6 but no change in IFN-β?
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A: This typically indicates that your response leans more towards an
NF-κB-driven pro-inflammatory program rather than a robust IRF3/7–type I interferon axis. It could also
be that the sampling time point did not capture the peak of IFN-β (it is recommended to extend the
IFN-related sampling window to cover 6–24 hours).
Q: Does undetectable IL-1β indicate the absence of inflammasomes?
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A: Not necessarily. The release of IL-1β/IL-18 depends on "processing and
maturation," which in many cases requires an appropriate secondary signal or a suitable time window. It
is recommended to simultaneously check: whether the stimulation intensity is sufficient, whether the
4–24-hour window is covered, and whether the sample type is appropriate (cell supernatants are usually
more sensitive).
Q: Should I use cell supernatant or serum/plasma for innate immune activation assessment?
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A:
- Mechanism Study: Prioritize cell supernatant for a cleaner background
and clearer signal source.
- Systemic Response/Pharmacodynamics and Toxicology/Cohort
Stratification: Priority: Serum/Plasma, more closely reflecting the overall inflammatory
burden.
- Local tissue reaction: Tissue homogenate/lysis buffer can be used, but
attention should be paid to normalization and matrix interference.
Q: If I can only choose 2 metrics, how can I avoid biased conclusions?
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A: Prefer "one strong signal + one directional indicator signal":
- Pro-inflammatory direction: TNF-α + IL-6
- Antiviral direction: IFN-β + CXCL10 can simultaneously address "how
strong" and "which axis is more biased," making misjudgment less likely compared to measuring
only one indicator.
Q: If I observe an increase in IL-10, what does this indicate? Does it represent "resolution" or
"immunosuppression"?
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A: An increase in IL-10 indicates enhanced negative feedback/regulation, but
it alone cannot independently prove "successful resolution." It is recommended to include IL-10 in the
enhanced version and compare it concurrently with TNF-α/IL-6.
