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*
The Biomedical Research Centre and
Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Despite the abundance of CD43 on the surface of leukocytes only moderate phenotypes were revealed in CD43 knockout mice. T cells from CD43null mice exhibited increased homotypic aggregation (11, 12, 13), and CD43null T cells were reported to exhibit a hyperproliferative response upon stimulation with a variety of mitogenic stimuli including CD3 ligation, Con A, staphylococcal enterotoxin B (SEB),3 and alloantigen (11). These results suggested that CD43 expression had a substantial impact on T cell responsiveness. Enhanced T cell adhesiveness and responsiveness have been the two primary phenotypic consequences associated with the CD43null mouse to date (10).
Although CD43null mice lacked gross impairment in T cell development, the reported hyperresponsive phenotype and increased adhesiveness led us to examine whether thymic selection events were affected in CD43null mice. To this end we used a TCR transgenic model where these processes had been well characterized and where modulation of CD43 glycoform expression during positive selection had been previously observed (14). We mated CD43null mice with mice expressing a male Ag (HY)-specific TCR transgene. Thymocytes bearing the HY-transgenic TCR are positively selected in female mice (15, 16) and negatively selected in male mice (15, 17). We found that neither positive nor negative thymic selection in HY-TCR mice was influenced by the absence of CD43. In vitro responsiveness of CD43null HY lymph node (LN) cells to mitogenic stimulation was also assessed to illustrate a dichotomy between lack of CD43 effect on thymic selection and the reported hyperresponsive phenotype previously associated with CD43null mice. Surprisingly, we did not observe a clear and consistent hyperresponsive pattern in HY CD43- vs HY CD43+ littermates. These observations challenged the original conclusions associating absence of CD43 with T cell hyperresponsiveness (11) and prompted us to re-examine this association in non-HY mice. Specifically, we examined whether the hyperresponsive phenotype was maintained under conditions where the potential contribution of strain 129-derived background genes was minimized. When LN cells from littermates of C57BL/6 backcrossed CD43+ and CD43null mice were compared there was no evidence of hyperresponsiveness associated with CD43 loss.
In summary, our results indicate that development of male Ag-specific CD8 T cells proceeds normally in the absence of CD43, and that T cells carrying the CD43null mutation on a C57BL/6 background are not hyperresponsive. Our results also highlight complications in the analysis of gene-knockout phenotypes in mixed background mice.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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The CD43-/- and CD43+ (control) mouse lines were generated as previously described (11). Briefly, the 129/terSv (H-2b)-derived embryonic stem cell line J1 (18) carrying the CD43-/- mutation was used to generate founder 129/CD43-/- mice. These CD43-/- founders were mated with CD43+/+ C57BL/6 (H-2b) mice to generate F1 hybrid mice with the CD43+/- genotype. Heterozygous F1 siblings were then mated to generate CD43-/-, CD43+/-, and CD43+/+ F2 offspring. The CD43-/- and CD43+/+ F2 mice were separated and intercrossed to generate what we refer to as the 129/CD43-/- and 129/CD43+/+ (control) lines, respectively. These lines were maintained by sibling mating. B6.CD43-/- mice referred to in this study were generated by Dr. Anne Sperling (University of Chicago, Chicago, IL) by crossing 129/CD43-/- mice with C57BL/6 for six generations. The CD43null mutation was maintained in successive generations by PCR typing using the following primers: CD43 sense: 5'-GGGGCCCTCGACTGAGATGC-3'; CD43 antisense: 5'-GGAGCAGATTG GATGAATACCTGTTGC-3'. Neo sense: 5'-CTTGTTGCCCCCTGCCCCTGATGT-3'; Neo antisense: 5'-GGGCGCCCGGTTCTTTTTGTCAAGACC-3'. F6 CD43+/- heterozygotes were then intercrossed to generate F6 B6.CD43-/- mice. These mice were provided by Dr. Jonathan Green (Washington University School of Medicine, St. Louis, MO) (19). To assess responsiveness in mice that shared maximal genetic identity but differed in CD43 expression, we bred these F6 B6.CD43-/- mice again with C57BL/6 to generate CD43+/- F7 heterozygotes. These heterozygotes were then backcrossed with F6 B6.CD43-/- yielding siblings with the CD43-/- genotype or the CD43+/- genotype that were used for comparisons of in vitro T cell responsiveness to various mitogenic stimuli. Responsiveness of CD43+/+ vs CD43+/- mice were also compared. For these analyses, offspring from F8 CD43+/- heterozygous mice were generated. The genotypes of CD43+/+ and CD43+/- sibling offspring were determined by PCR, using the primers indicated above, and confirmed by flow cytometry with anti-CD43 (S7-PE, no. 01605B; PharMingen). To examine the effects of CD43 on positive and negative selection processes, homozygous HY TCR-transgenic mice on the C57BL/6 background (16) were mated with 129/CD43-/-. HY+CD43+/- and HY+CD43-/- offspring were produced from HY+CD43-/- x HY+CD43+/- matings. Offspring were typed with S7-PE and the TCR clonotypic Ab T3.70 (16). These mice were used for the analysis of CD43 effects on thymic selection events in male or female mice. Mice aged 9–16 wk were used for analyses.
Antibodies
MAb 145-2C11 (20) was used for in vitro stimulation
and is a hamster Ab specific for CD3
. S7-PE specific for the
tetrasaccharide form of CD43 (6) was used to type mice for
CD43 status. Other Abs included CD4-PE (09005B; PharMingen) and
CD8-FITC (01044D; PharMingen). T3.70-FITC mAb specific for the
HY-transgenic TCR 
-chain (17) was FITC conjugated in
our laboratory.
Media and culture conditions
Cell suspensions were prepared in RPMI 1640 medium (Life Technologies, Grand Island, NY) supplemented with 5% FCS and cultured in Iscove’s medium (cat. no. 12200-085; Life Technologies) supplemented with 10% FCS, 5 x 10-5 M 2-ME, antibiotics 100 U/ml each of penicillin and streptomycin (Stem Cell Technologies, Paisley, U.K.), and 2 mM glutamine (Sigma, St. Louis, MO). Where indicated, cultures also included Con A (C-0412; Sigma), SEB (S-4881; Sigma), or 145-2C11 Ab at the concentrations specified. Dendritic cell preparations were isolated from spleen by differential adherence as previously described (21), irradiated with 2000 rad, and included at 104 per well where indicated.
Flow cytometry
For cell surface staining, cells were suspended in PBS containing 2% (v/v) FCS and incubated with Abs for 20–40 min on ice in 96-well round-bottom plates (Nunclon InterMed, Roskild, Denmark). Cells were washed twice and analyzed on a FACScan IV flow cytometer (Becton Dickinson, Mountain View, CA).
Proliferation assays
LN cells (105) in 150 µl medium were
stimulated with indicated amounts of either Con A-, 2C11-, SEB-, or
2000R-irradiated stimulator cells from male, female, or allogeneic
(BALB/c, H-2d) mice. Cell stimulation was
evaluated by using either a flow cytometer-based bead assay or by
tritiated thymidine ([3H]Thy) incorporation of
triplicate or quadruplicate replicate cultures. For the bead assay
(22, 23, 24), 100 µl of the 150-µl cell culture was
harvested at the times indicated and combined with an equal volume of
PBS containing 2 µg/ml propidium iodide and 4-micron-diameter latex
beads at a concentration of 2 x 106/ml
(cat. no. 2-4000; Interface Techniques, Cambridge, MA). Dead cells
stained with propidium iodide (FL3high) were excluded from
analysis on the basis of forward light scatter x FL3 gating.
Latex beads, viable small lymphocytes, and blasts (large cells) were
then easily resolved on the basis of forward light scatter and
side light scatter characteristics. Ratios of latex beads to blasts
were obtained by gated analysis with CellQuest software (Becton
Dickinson). Using Microsoft Excel software and the ratio of
blasts/beads, blast cell yields were determined for each 100-µl
culture aliquot from triplicate or quadruplicate cultures. Tritiated
thymidine incorporation was also used to evaluate responsiveness and to
confirm the validity of the flow cytometer-based bead assay. For these
analyses 150 microliter cell cultures were split, and one aliquot was
evaluated by bead assay while the other aliquot was pulsed with
tritiated thymidine and harvested 6 h later. In regard to assay
validity, (also refer to Fig. 3
) there was good concurrence in response
assessments based on visual inspection of individual wells before
harvesting, thymidine incorporation, and bead assay.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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To monitor the effects of CD43 expression on T cell selection,
we analyzed CD43null and
CD43+/- heterozygous mice expressing the 
TCR genes specific for male Ag (HY) presented by the class I MHC
molecule H-2Db (15). In female mice
expressing the HY TCR transgene, positive selection of CD8 cells
expressing the transgenic TCR is reflected in the intrathymic
accumulation of substantial numbers of
CD4-CD8+ thymocytes. These
thymocytes express high levels of the transgenic TCR, are male
Ag-reactive, and are exported to peripheral lymphoid tissues
(16). In contrast, TCR-transgenic
CD4+8+ thymocytes
developing in male mice encounter male Ag in the thymus and are subject
to negative selection, resulting in a gross reduction in thymocyte
numbers and as a consequence, HY-TCR-transgenic male mice lack
male-Ag-reactive CD8 T cells in the periphery (15, 17).
Therefore, analysis of T cell subsets in thymi and LNs from male and
female HY+ CD43+ and
HY+ CD43- transgenic mice
should provide insight into CD43 influence on negative and positive
selection processes, respectively.
The outcome of thymic maturation in the presence or absence of CD43 was
monitored by both flow cytometry and functional assays. As shown in
Fig. 1A, accumulation of
CD4-8+ thymocytes in HY
mice was not affected by CD43 status. LN cells similarly showed no
evidence of CD4/8 profile perturbation associated with the absence of
CD43. TCR expression in both thymus and LN was similarly unaffected by
the absence of CD43. There was also no significant difference in
thymocyte yields among female HY+
CD43+ and HY+
CD43- mice. There was some variability in the
level of CD8 staining observed on
CD4-8+ thymocytes. When
multiple experiments were conducted, this variability did not correlate
with the presence or absence of CD43. We suspect that variations in CD8
staining may have resulted from the fact that mice analyzed included
individuals that were either heterozygous or homozygous for the HY TCR.
Expression of CD5 and CD69 were also assessed. Expression of CD5 may be
a good measure of productive TCR-MHC engagement in thymic
subpopulations (25), and CD69 is an early activation
marker that is also differentially expressed in thymocytes
(26). Neither CD5 nor CD69 expression were influenced by
the absence of CD43 in either
CD4+8+ or positively
selected CD4-8+ thymocytes
(data not shown).
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B, CD4+8+ cells
were effectively and comparably deleted in CD43+
and CD43- thymi. Thymocyte yields were 2–5
x 106 cells and were not significantly different
in CD43+ vs CD43- mice. No
effect of CD43 deficiency was apparent on CD4/8 staining or TCR
expression on the peripheral T cell pool in male mice expressing the
transgenic TCR (Fig. 1C). Male Ag-reactive T cells develop normally in HY CD43null mice
To reinforce the conclusion that positive selection of male
Ag-specific T cells had occurred normally in HY female
CD43-/- mice, LN T cells were harvested and
stimulated with preparations of male splenic dendritic cells.
Stimulation with 2C11 (anti-CD3) and Con A were conducted in
parallel to monitor whether general T cell responsiveness was affected
by CD43 deficiency in HY mice; hyperresponsiveness of
129/CD43-/- mice to these mitogenic stimuli had
been described previously (11). As shown in Fig. 2, there was no evidence of altered male
Ag-specific responsiveness in female HY CD43-/-
vs HY CD43+/+ mice. Thus, by phenotypic and
functional criteria, male Ag-reactive T cells had undergone comparable
positive selection in both female HY CD43+ and HY
CD43- mice. Surprisingly, we did not observe a
clear pattern of hyperresponsiveness among HY
CD43-/- mice to either male Ag or mitogen
stimulation, prompting us to re-examine the hyperresponsive phenotype
thought to be associated with T cells from
CD43null mice.
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To re-examine the hyperresponsive phenotype we resorted to the
129/CD43-/- and
129/CD43+/+ mouse lines originally generated from
F2 offspring from founder
CD43null mice (see Materials and
Methods). We conducted extensive analysis of mitogen
responsiveness of peripheral T cells and found that LN cells from
129/CD43null mice frequently, but inconsistently,
displayed a hyperresponsive phenotype. An example of one experiment
shown in Fig. 3A illustrated
the variability frequently observed in responsiveness to mitogen. LN
cells from three 129/CD43-/- mice and three
129/CD43+/+ control mice were stimulated with SEB
as indicated. LN cells from one of the 129/CD43-
mice exhibited an elevated response pattern to SEB in the range of that
originally described (11), whereas the response of the
other two 129/CD43null littermates were not
significantly different from the responses obtained for
129/CD43+ LN cells. A similar response pattern
was also observed after stimulation with either Con A or 2C11 (data not
shown).
When substantial variation in mitogen responsiveness occurred, this
variation was evident by simple microscopic examination as well as by
cytometry-based counting and thymidine incorporation. In several
experiments both flow cytometry-based cell counting methods and
thymidine incorporation were conducted in parallel to confirm that
these two methods were consistent with each other and would similarly
detect relevant response variations (Fig. 3B). Importantly,
these analyses established that measurements of T cell responsiveness
by flow cytometry were comparable to those based on thymidine
incorporation that had been used in the original study of CD43
responsiveness (11).
B6.CD43null mice do not exhibit a hyperresponsive phenotype
Poor consistency in reproducing a hyperresponsive phenotype in
LN cells from 129/CD43null mice suggested that
CD43-independent genetic variation arising from their breeding history
might be relevant to the hyperresponsive phenotype originally ascribed
to CD43. To investigate this possibility, we obtained
CD43-/- mice that had been backcrossed onto the
C57BL/6 background for six generations. Using these mice, litters were
generated that contained 
50% CD43-/- mice
and 50% CD43+/- mice (see Materials and
Methods), and LN cells from these littermates were then examined
for responsiveness to mitogen stimulation. Use of littermates from B6
backcrossed mice minimized the possibility that CD43-independent
factors would influence responsiveness. A representative set of results
from one litter is shown in Fig. 4 and
demonstrates that CD43 does not affect T cell responsiveness to Con A,
SEB, 2C11, or allo-Ag, even when limiting amounts of mitogen were used.
Three litters of mice, each from three different sets of parents, were
analyzed with comparable results. Thus we did not observe response
differences in LN cells from CD43-expressing
(CD43+/-) heterozygotes and
CD43-/- deficient mice.
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, we
observed no significant differences in mitogenic responses of
CD43+/- and CD43+/+
littermates. Thus, within the limits of our experimental analysis of
CD43 deficiency in littermates on the B6 background we find that CD43
loss in either the heterozygote (+/-) or homozygote (-/-) condition
does not confer T cell hyperresponsiveness to mitogenic stimuli.
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Our observation that B6.CD43null mice lack the T cell hyperresponsive phenotype raises questions about the basis of the hyperresponsiveness originally observed in 129/CD43null mice and whether CD43, in fact, has any direct bearing on T cell activation or responsiveness. Clarification of the involvement of CD43 in T cell responsiveness is important given the magnitude of the effects ascribed to its loss (11).
The original assessment of T cell responsiveness of CD43null mice was based upon F2 offspring of founder 129/CD43null and C57BL/6 mice (11) (described in Materials and Methods). The genetic backgrounds of individual F2 siblings would be expected to be profoundly different due to random segregation of 129-derived and B6-derived chromosomes in individual F2 mice. Therefore, analysis of F2 mice and, particularly, CD43+/+ and CD43-/- mouse lines derived from them could be confounded by genetic background differences. Indeed, such genetic variation may have been responsible for variable hyperresponsiveness we observed in some 129/CD43-/- mice similar to that originally reported. Moreover, strain 129-associated hyperresponsiveness relative to B6 has recently been observed both in vitro and in vivo using a transgenic autoimmune model of diabetes.4
The only reliable way to ascribe any phenotype to loss of CD43 among F2 siblings requires that a sufficient number of CD43+ and CD43- siblings be examined; only if a given phenotype segregates consistently with the absence of CD43 in all F2 mice can the association between the phenotype and CD43 loss be tentatively established. Such an association must be regarded as tentative because the influence of background genes (in this case of 129 origin) that are physically linked to the site of the null mutation would not have been considered.
It is clear from the analysis described in this report that the CD43null mutation is not associated with hyperresponsiveness on the B6 genetic background, whereas observations of hyperresponsiveness were originally described in mice with a 129 x B6 background (11). The variable expression of hyperresponsiveness we observed among 129/CD43-/- mice and the absence of a CD43-dependent hyperresponsiveness among siblings of B6 backcrossed mice lead us to conclude that the absence of CD43 does not confer T cell hyperresponsiveness to mitogenic stimuli on the C57BL/6 background and to ascribe hyperresponsiveness originally associated with the absence of CD43 to influence of C57BL/6 vs 129 genetic backgrounds. Such genetic influences could be multigenic in origin and could include positive effects contributed by 129 genes or negative effects contributed by C57BL/6 genes.
Our observations do not exclude all possibility that CD43 could influence T cell responsiveness under certain conditions. Considering the abundance, topology, and charge associated with CD43, it is perhaps not surprising that overexpression or absence of CD43 could influence T cell biology in a variety of ways; this perspective could account for the fact that, with the exception of data on CD43 function in adhesion (7, 9, 11, 12, 13), the literature on proposed CD43 function lacks a clear unified theme. The real challenge posed by CD43 is to accurately discriminate between those effects that are of physiological importance and those that are not. In this context, the CD43null mouse continues to represent an important tool in dissecting CD43 function. Finally, our analysis serves as one example of the complexity of genetics and phenotyping that can plague the analysis of knockout mice on a mixed genetic background.
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Acknowledgments |
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Footnotes |
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2 Address correspondence and reprint requests to Dr. Hermann Ziltener, The Biomedical Research Center, University of British Columbia, 2222 Health Sciences Mall, Vancouver, British Columbia V6T-1Z3 Canada.
3 Abbreviations used in this paper: SEB, staphylococcal enterotoxin B; LN, lymph node.
4 Garza, K. M., K. J. McKall-Faienza, A. Zakarian, B. Odermatt, and P. S. Ohashi. Enhanced T-cell responses contribute to the genetic predisposition of CD8-mediated spontaneous autoimmunity. Submitted for publication.
Received for publication July 21, 2000. Accepted for publication October 9, 2000.
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References |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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T-cell receptor determine the CD4/CD8 phenotype of T cells. Nature 335:229.[Medline]
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