Abstract
Among many challenges facing the battle against infectious disease, one quandary stands out. On the one hand, it is often unclear how well animal models and cell lines mimic human immune behavior. On the other hand, many core methods of cell and molecular biology cannot be applied to human subjects. For example, the profound susceptibility of neutropenic patients to infection marks neutrophils (the most abundant white blood cells in humans) as vital immune defenders. Yet because these cells cannot be cultured or genetically manipulated, there are gaps in our understanding of the behavior of human neutrophils. Here, we discuss an alternative, interdisciplinary strategy to dissect fundamental mechanisms of immune-cell interactions with bacteria and fungi. We show how biophysical analyses of single-live-cell/single-target encounters are revealing universal principles of immune-cell phagocytosis, while also dispelling misconceptions about the minimum required mechanistic determinants of this process.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 469-476 |
| Number of pages | 8 |
| Journal | Biophysical Journal |
| Volume | 109 |
| Issue number | 3 |
| DOIs | |
| State | Published - Aug 6 2015 |
Fingerprint
ASJC Scopus subject areas
- Biophysics
Cite this
Controlled One-on-One Encounters between Immune Cells and Microbes Reveal Mechanisms of Phagocytosis. / Heinrich, Volkmar.
In: Biophysical Journal, Vol. 109, No. 3, 06.08.2015, p. 469-476.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Controlled One-on-One Encounters between Immune Cells and Microbes Reveal Mechanisms of Phagocytosis
AU - Heinrich, Volkmar
PY - 2015/8/6
Y1 - 2015/8/6
N2 - Among many challenges facing the battle against infectious disease, one quandary stands out. On the one hand, it is often unclear how well animal models and cell lines mimic human immune behavior. On the other hand, many core methods of cell and molecular biology cannot be applied to human subjects. For example, the profound susceptibility of neutropenic patients to infection marks neutrophils (the most abundant white blood cells in humans) as vital immune defenders. Yet because these cells cannot be cultured or genetically manipulated, there are gaps in our understanding of the behavior of human neutrophils. Here, we discuss an alternative, interdisciplinary strategy to dissect fundamental mechanisms of immune-cell interactions with bacteria and fungi. We show how biophysical analyses of single-live-cell/single-target encounters are revealing universal principles of immune-cell phagocytosis, while also dispelling misconceptions about the minimum required mechanistic determinants of this process.
AB - Among many challenges facing the battle against infectious disease, one quandary stands out. On the one hand, it is often unclear how well animal models and cell lines mimic human immune behavior. On the other hand, many core methods of cell and molecular biology cannot be applied to human subjects. For example, the profound susceptibility of neutropenic patients to infection marks neutrophils (the most abundant white blood cells in humans) as vital immune defenders. Yet because these cells cannot be cultured or genetically manipulated, there are gaps in our understanding of the behavior of human neutrophils. Here, we discuss an alternative, interdisciplinary strategy to dissect fundamental mechanisms of immune-cell interactions with bacteria and fungi. We show how biophysical analyses of single-live-cell/single-target encounters are revealing universal principles of immune-cell phagocytosis, while also dispelling misconceptions about the minimum required mechanistic determinants of this process.
UR - http://www.scopus.com/inward/record.url?scp=84938511740&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84938511740&partnerID=8YFLogxK
U2 - 10.1016/j.bpj.2015.06.042
DO - 10.1016/j.bpj.2015.06.042
M3 - Article
AN - SCOPUS:84938511740
VL - 109
SP - 469
EP - 476
JO - Biophysical Journal
JF - Biophysical Journal
SN - 0006-3495
IS - 3
ER -